PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32592377-10 2020 The upregulation of caspase 3 and downregulation of VEGF mRNA were observed in double combinations of NVP-AUY922 and DOX versus single treatments. Doxorubicin 117-120 caspase 3 Homo sapiens 20-29 32185414-8 2020 Interestingly, the compound 3i-1000 attenuated doxorubicin-induced increase in pro-B-type natriuretic peptide (proBNP) expression and caspase-3/7 activation in hiPSC-CMs. Doxorubicin 47-58 caspase 3 Homo sapiens 134-143 31833715-6 2020 Materials and Methods: The cytotoxic and apoptotic effect of Methylstat and Doxorubicin on HL-60 was detected by MTT cell viability assay, Double Staining of Treated Cells with Annexin-V/ Propidium Iodide (PI), and Caspase-3 Activity Assay, respectively. Doxorubicin 76-87 caspase 3 Homo sapiens 215-224 32032743-8 2020 Caspases 3/7 and 9 activity assay revealed the involvement of hsa-miR-766-5p in mitochondrial apoptosis pathway regulation detected following overexpression and downregulation of this miRNA, detected in SW480 cells treated with 1muM doxorubicin. Doxorubicin 233-244 caspase 3 Homo sapiens 0-18 32308718-15 2020 The apoptotic enzyme caspase-3 was induced in a concentration dependent manner upon treatment of the RD cells with SAHA extracts or doxorubicin. Doxorubicin 132-143 caspase 3 Homo sapiens 21-30 32145585-7 2020 Our results showed that Dox-induced damage in HUVECs were reduced through Kae to promote the expression of total protein 14-3-3gamma and mitochondrial Bcl-2, phosphorylate Bad, increase cell viability, NO content, DDAHIIactivity, p-eNOS/eNOS ratio, and MMP levels, maintained NAD+/NADH and GSH/GSSG balance, and decrease LDH and caspase-3 activities, ADMA content, ROS generation, mPTP openness, and apoptosis. Doxorubicin 24-27 caspase 3 Homo sapiens 329-338 31843629-6 2020 The combination of DOX and PA-2 remarkably increases the release of cytochrome C and the activation of caspase-3 and caspase-9, compared with DOX treatment alone. Doxorubicin 19-22 caspase 3 Homo sapiens 103-112 31885804-10 2019 Our results showed that Dox-induced injury to vascular endothelium was decreased by TMP via upregulating 14-3-3gamma expression in total protein and Bcl-2 expression in mitochondria, activating Bad (S112) phosphorylation, maintaining EDD, reducing LDH, CK, and caspase-3 activities, thereby causing a reduction in apoptotic rate, and histopathological changes of vascular endothelium (in vivo). Doxorubicin 24-27 caspase 3 Homo sapiens 261-270 31707337-10 2020 Additionally, DOX/Mag combinational treatment significantly induced apoptosis in breast cancer cells when compared to DOX alone group through inducing Caspase-3 cleavage. Doxorubicin 14-17 caspase 3 Homo sapiens 151-160 31563593-4 2019 In the DOX-resistant cancer cells, degree of autophagy elicited by DOX was milder than the parental cells, and DOX treatment hardly activated the ROS-dependent apoptotic signals [formation of 4-hydroxy-2-nonenal (HNE), cytochrome-c release into cytosol, and activation of JNK and caspase-3], inferring an inverse correlation between cellular antioxidant capacity and autophagy induction by DOX. Doxorubicin 7-10 caspase 3 Homo sapiens 280-289 31319070-7 2019 DOX markedly increased reactive oxygen species production, p53 expression, caspase-3 activity, cleaved caspase-3 levels, and TUNEL-positive cell numbers but reduced Bcl-2 expression and intracellular antioxidant enzyme levels; these effects were effectively antagonized through nicorandil (3 muM, 12 h) pretreatment, which resulted in HUVECs being protected from DOX-induced apoptosis. Doxorubicin 0-3 caspase 3 Homo sapiens 75-84 33405660-7 2019 At the same time, the obtained results demonstrate the possibility of regulating the initiation of apoptosis or necrosis in tumor cells after treatment with different concentrations of DOX-PSi NPs, as revealed by the analysis of the caspase-3 processing, the accumulation of sub-G1 cell fraction, and morphological changes determined by electron and light microscopy. Doxorubicin 185-188 caspase 3 Homo sapiens 233-242 31445005-5 2019 METHODS AND RESULTS: In vitro and in vivo experiments showed that DOX treatment induced cardiomyocyte pyroptosis as evidenced by increased cell death and upregulated expression levels of NLR family pyrin domain containing 3 (NLRP3), caspase-3, IL-1beta, IL-18 and GMDSD-N. Doxorubicin 66-69 caspase 3 Homo sapiens 233-242 31571866-7 2019 Pronounced anti-migratory activity, DNA fragmentation, decrease in expression of procaspase-3 and enhancement of p53 expression were further identified upon exposure to surface-coated IONs with tethered doxorubicin and ellipticine. Doxorubicin 203-214 caspase 3 Homo sapiens 81-93 31319070-7 2019 DOX markedly increased reactive oxygen species production, p53 expression, caspase-3 activity, cleaved caspase-3 levels, and TUNEL-positive cell numbers but reduced Bcl-2 expression and intracellular antioxidant enzyme levels; these effects were effectively antagonized through nicorandil (3 muM, 12 h) pretreatment, which resulted in HUVECs being protected from DOX-induced apoptosis. Doxorubicin 0-3 caspase 3 Homo sapiens 103-112 30609135-7 2019 The results of the present study demonstrated that treatment of SKOV3 with 55 muM of RES and 250 nM of DOX simultaneously increased cell viability in CSCs to DOX after 24 and 48 hours by increasing the expression of Bcl-2-associated X protein (BAX) and caspase-3 genes, and decreased the expression and function of multidrug resistance protein 1 (MDR1) and multidrug resistance-associated protein 1 (MRP1) genes indicated by intracellular the rhodamine 123 content. Doxorubicin 103-106 caspase 3 Homo sapiens 253-262 31128433-6 2019 Compounds 7, 9, 15, 16, 21 and 22 increased the level of active caspase 3 by 4-8 folds, compared to the control cells in MCF-7 cell line and doxorubicin as a reference drug. Doxorubicin 141-152 caspase 3 Homo sapiens 64-73 31202781-4 2019 Dox plus Ori synergistically induced apoptosis in MDA-MB-231 cells, in a manner involving regulation of the Bcl-2/Bax, PARP, Caspase 3 and Survivin signaling pathways. Doxorubicin 0-3 caspase 3 Homo sapiens 125-134 31132617-4 2019 Doxil-treated cells exhibited 3.38-fold higher caspase-3 levels than control cells, while doxorubicin significantly increased caspase-3 levels by 2.72-fold. Doxorubicin 0-5 caspase 3 Homo sapiens 47-56 31132617-4 2019 Doxil-treated cells exhibited 3.38-fold higher caspase-3 levels than control cells, while doxorubicin significantly increased caspase-3 levels by 2.72-fold. Doxorubicin 90-101 caspase 3 Homo sapiens 126-135 30988617-8 2019 Mechanistic studies suggested that P-LPNs enhanced DOX cytotoxicity by increased release of cytochrome c and enhanced caspase3 cleavage, causing apoptosis in HepG2/ADR cells. Doxorubicin 51-54 caspase 3 Homo sapiens 118-126 31401980-9 2019 Overexpression of ACOX1 alleviated doxorubicin-induced activation of caspase-9 and caspase-3 and decrease of mitochondrial membrane potential. Doxorubicin 35-46 caspase 3 Homo sapiens 83-92 30659905-0 2019 The novel strategy for concurrent chemoradiotherapy by conjugating the apoptotic cell-binding moiety to caspase-3 activated doxorubicin prodrug. Doxorubicin 124-135 caspase 3 Homo sapiens 104-113 33418833-5 2018 We found that the percentage of cleaved Caspase-3 positive cells was significantly lower in the bioprinted constructs with ADMSC and 21PT than that in the cancer cell alone constructs, in response to low DOX dose. Doxorubicin 204-207 caspase 3 Homo sapiens 40-49 30387987-5 2018 The ARPI-derived bioactive peptides exhibit synergistic anticancer effect with DOX by regulating pro- and antiapoptotic-relevant proteins ( p53, Bax, Bcl-2, pro-caspase-3) at mitochondria. Doxorubicin 79-82 caspase 3 Homo sapiens 157-170 30485942-5 2018 Expression of proapoptoticproteins (caspases 3 and 9) was up-regulated upon administration of tyloporine alone or in combination with doxorubicin.Conclusions: Tylophorine alone or in combination with doxorubicin induced apoptosis in T47D breast cancer cellsthrough modulation of the cell cycle and affecting the expression of caspases 3 and 9. Doxorubicin 134-145 caspase 3 Homo sapiens 36-52 30485942-5 2018 Expression of proapoptoticproteins (caspases 3 and 9) was up-regulated upon administration of tyloporine alone or in combination with doxorubicin.Conclusions: Tylophorine alone or in combination with doxorubicin induced apoptosis in T47D breast cancer cellsthrough modulation of the cell cycle and affecting the expression of caspases 3 and 9. Doxorubicin 134-145 caspase 3 Homo sapiens 326-342 30485942-5 2018 Expression of proapoptoticproteins (caspases 3 and 9) was up-regulated upon administration of tyloporine alone or in combination with doxorubicin.Conclusions: Tylophorine alone or in combination with doxorubicin induced apoptosis in T47D breast cancer cellsthrough modulation of the cell cycle and affecting the expression of caspases 3 and 9. Doxorubicin 200-211 caspase 3 Homo sapiens 36-52 30483812-11 2019 Immunoblotting demonstrated that levistolide A enhanced doxorubicin-induced cell death by decreasing the expression levels of B-cell lymphoma 2 and increasing caspase 3 expression. Doxorubicin 56-67 caspase 3 Homo sapiens 159-168 29914576-13 2018 In addition, it also potentiated the cytotoxic activities and inhibitory activities of 5-FU and DOX on cell migration through induction of cell apoptosis and activation of caspase 3/7. Doxorubicin 96-99 caspase 3 Homo sapiens 172-181 30388099-8 2018 Cotreatment of DHC enhanced the apoptosis-inducing effects of DOX by activating caspase-9 and caspase-3 followed by cleavage of PARP. Doxorubicin 62-65 caspase 3 Homo sapiens 94-103 29959912-6 2018 Here, we show that SAHA and doxorubicin markedly enhance the cleavage of two apoptosis markers, caspase 3 and poly-ADP ribose polymerase (PARP-1), and increase the phosphorylation of gammaH2AX, a marker of DNA damage. Doxorubicin 28-39 caspase 3 Homo sapiens 96-105 30181466-6 2018 Our results showed that DOX-Vit D, but not DOX, significantly elicited an apoptotic signal in MG63 cells as evidenced by induction of death receptor, Caspase-3 and BCLxs genes. Doxorubicin 24-27 caspase 3 Homo sapiens 150-159 30266241-8 2018 Moreover, metformin could elevate DOX-induced apoptosis in DU145 cells in a concentration-dependent manner and DOX-induced caspase-3 activity. Doxorubicin 111-114 caspase 3 Homo sapiens 123-132 30217455-7 2018 4-HBA significantly promoted the anticancer effect of ADM on apoptosis induction, as evidenced by the increased expressions of Caspase-3 and PARP cleavage, which was associated with the promotion p53 and homeodomain interacting protein kinase-2 (HIPK2) expressions in ADM-resistant breast cancer cells. Doxorubicin 54-57 caspase 3 Homo sapiens 127-136 29655913-6 2018 Adriamycin induced the apoptosis and caspase-3 activity of K562/ADM cells, and the germacrone treatment significantly enhanced the induction. Doxorubicin 0-10 caspase 3 Homo sapiens 37-46 28844998-9 2017 In addition, BUF combined with DOX could block the cell stage of A549 cells, keep the cell stage stay in S stage and up-regulate the expression of caspase-3. Doxorubicin 31-34 caspase 3 Homo sapiens 147-156 29749767-3 2018 Compounds 7a, 8a, 8d, 14a and 14d were superior to doxorubicin as activators of caspases 3, 8 and 9 in HCT-116 cell line. Doxorubicin 51-62 caspase 3 Homo sapiens 80-99 29254044-4 2018 Mechanistic studies suggested that DOX-SeNPs@TMC-FA induced cell death through the apoptosis pathway by involvement of caspase-3 and PARP proteins. Doxorubicin 35-38 caspase 3 Homo sapiens 119-128 29098037-7 2017 It was also demonstrated that doxorubicin, an anticancer agent, reduced cell viability, induced a significant increase in the B-cell lymphoma (Bcl)-2 associated X protein (Bax)/Bcl-2 ratio and decreased pro-caspase-3 levels in wild-type HepG2 cells. Doxorubicin 30-41 caspase 3 Homo sapiens 203-216 28666101-3 2017 CFUNs were formulated from the self-assembly of caspase-3 responsive doxorubicin (DOX) prodrug tethered with DEVD peptide (DEVD-DOX), upconversion nanoparticles (UCNP), a photosensitizer (pyropheophorbide-a methyl ester, MPPa), and tumor-targeting cRGD-PEG-DSPE to afford multifunctional CFUNs, MPPa/UCNP-DEVD-DOX/cRGD. Doxorubicin 69-80 caspase 3 Homo sapiens 48-57 28666101-3 2017 CFUNs were formulated from the self-assembly of caspase-3 responsive doxorubicin (DOX) prodrug tethered with DEVD peptide (DEVD-DOX), upconversion nanoparticles (UCNP), a photosensitizer (pyropheophorbide-a methyl ester, MPPa), and tumor-targeting cRGD-PEG-DSPE to afford multifunctional CFUNs, MPPa/UCNP-DEVD-DOX/cRGD. Doxorubicin 82-85 caspase 3 Homo sapiens 48-57 28666101-4 2017 Upon cellular uptake and NIR irradiation, the visible light emission of UCNP could excite MPPa to produce reactive oxygen species for photodynamic therapy (PDT) along with the activation of caspase-3, which further cleaved DEVD peptide to release DOX within tumor cells, thus accomplishing NIR-triggered PDT and cascade chemotherapy. Doxorubicin 247-250 caspase 3 Homo sapiens 190-199 28627658-0 2017 Shikonin promotes adriamycin-induced apoptosis by upregulating caspase-3 and caspase-8 in osteosarcoma. Doxorubicin 18-28 caspase 3 Homo sapiens 63-72 29494960-13 2018 Moreover, I3C attenuate DOX-induced apoptosis by up-regulation of Bcl2 and down-regulation of Bax and caspase-3 expression in bone marrow cells. Doxorubicin 24-27 caspase 3 Homo sapiens 102-111 29458045-7 2018 Further, fidarestat prevented the Dox-induced oxidative stress, formation of reactive oxygen species (ROS) and activation of Caspase-3 in HUVECs. Doxorubicin 34-37 caspase 3 Homo sapiens 125-134 29141199-6 2018 The combinatory strategy of MitoK3 with anticancer agent doxorubicin (DOX) resulted in a degree of cytotoxicity higher than those of the individual molecules, as the combination triggered tumour apoptotic cell death evident by caspase 3/9 activities, probably through mitochondrial destabilization or by interference with mitochondrial redox processes. Doxorubicin 57-68 caspase 3 Homo sapiens 227-236 29141199-6 2018 The combinatory strategy of MitoK3 with anticancer agent doxorubicin (DOX) resulted in a degree of cytotoxicity higher than those of the individual molecules, as the combination triggered tumour apoptotic cell death evident by caspase 3/9 activities, probably through mitochondrial destabilization or by interference with mitochondrial redox processes. Doxorubicin 70-73 caspase 3 Homo sapiens 227-236 29113274-10 2017 Additionally, simvastatin in combination with doxorubicin significantly induced expression of the cyclin-dependent kinase inhibitor p21, increased cytochrome c and caspase 3 expression and reduced cyclin D1 expression. Doxorubicin 46-57 caspase 3 Homo sapiens 164-173 28844998-10 2017 : Conclusion: BUF combined with DOX can significantly inhibit the proliferation of A549 cells, which might be related to the induction of apoptosis, cell cycle S phase arrest and caspase-3 up-regulation. Doxorubicin 33-36 caspase 3 Homo sapiens 180-189 28476801-10 2017 Elevated levels of activated caspase-3 were observed only in AzaC/Dox group of cells. Doxorubicin 66-69 caspase 3 Homo sapiens 29-38 28498322-4 2017 Concurrently, the synergistic apoptotic cell death caused by the VPA and DOX combination treatment was confirmed by Hoechst nuclear staining and Western blot analysis of caspase-3 and poly (ADP-ribose) polymerase (PARP) activation. Doxorubicin 73-76 caspase 3 Homo sapiens 170-212 28476801-12 2017 CONCLUSION: AzaC significantly increases the sensitivity of MCF7 cells to Dox via activation of ERK1/2, P53, BAX and caspase-3. Doxorubicin 74-77 caspase 3 Homo sapiens 117-126 28314260-6 2017 Doxorubicin induced apoptosis (characterized by the loss of cell surface microvilli, chromatin condensation, nuclear fragmentation and caspase-3 activation) in keratinocytes. Doxorubicin 0-11 caspase 3 Homo sapiens 135-144 27863037-3 2017 Doxorubicin-incorporated multivalent aptamer-siRNA conjugates exert promising anticancer effects, such as activation of caspase-3/7 and decrease of cell viability, on multidrug-resistant cancer cells because of their high intracellular uptake efficiency. Doxorubicin 0-11 caspase 3 Homo sapiens 120-129 28971453-3 2017 The pretreatment with GR+U combined with doxorubicin (DOX) was evaluated from IC50, caspase-3 expression and mechanisms of cell death by electron microscopy. Doxorubicin 41-52 caspase 3 Homo sapiens 84-93 28222632-5 2017 CPT combined with DOXO induced apoptosis and cleavage of caspases-3,-7,-9 as well as PARP. Doxorubicin 18-22 caspase 3 Homo sapiens 57-73 28971453-3 2017 The pretreatment with GR+U combined with doxorubicin (DOX) was evaluated from IC50, caspase-3 expression and mechanisms of cell death by electron microscopy. Doxorubicin 54-57 caspase 3 Homo sapiens 84-93 28971453-9 2017 The caspase-3 level and ultraestructural analysis showed that treatment with GR+U+DOX enhances induction of apoptosis. Doxorubicin 82-85 caspase 3 Homo sapiens 4-13 27900057-16 2016 Overall, the combination of DHA and DOX markedly inhibited the viability of the HeLa, OVCAR-3, MCF-7, PC-3 and A549 cells, and acted on the HeLa cells through the intrinsic apoptotic pathway mediated by caspase-9 and caspase-3. Doxorubicin 36-39 caspase 3 Homo sapiens 217-226 28955990-7 2017 However, the cytotoxicity of doxorubicin was increased remarkably and accompanied with the caspase- 3 activation in the presence of 15d-PGJ2. Doxorubicin 29-40 caspase 3 Homo sapiens 91-101 27654264-6 2016 RESULTS: Paclitaxel and DOX decreased cell viability and increased caspase-3 activity, and co-treatment with VPA enhanced this effect. Doxorubicin 24-27 caspase 3 Homo sapiens 67-76 27487838-9 2016 Restoration and/or activation of TFEB in DOX-treated cardiomyocytes prevented DOX-induced suppression of cathepsin B activity, reduced DOX-mediated reactive oxygen species (ROS) overproduction, attenuated activation of caspase-3, and improved cellular viability. Doxorubicin 41-44 caspase 3 Homo sapiens 219-228 27487838-9 2016 Restoration and/or activation of TFEB in DOX-treated cardiomyocytes prevented DOX-induced suppression of cathepsin B activity, reduced DOX-mediated reactive oxygen species (ROS) overproduction, attenuated activation of caspase-3, and improved cellular viability. Doxorubicin 78-81 caspase 3 Homo sapiens 219-228 27487838-9 2016 Restoration and/or activation of TFEB in DOX-treated cardiomyocytes prevented DOX-induced suppression of cathepsin B activity, reduced DOX-mediated reactive oxygen species (ROS) overproduction, attenuated activation of caspase-3, and improved cellular viability. Doxorubicin 78-81 caspase 3 Homo sapiens 219-228 27154500-10 2016 Finally, the co-delivery of Dox and p53-pDNA using the copolymer displayed greater cytotoxic effect compared with the Dox-loaded nanoparticle counterpart as revealed by cell viability and Caspase 3 expression assay. Doxorubicin 28-31 caspase 3 Homo sapiens 188-197 27698706-4 2016 SPPC potentiated Dox-induced apoptosis in breast cancer cells via the mitochondrial apoptosis signaling pathway by activating caspase-3 and caspase-9. Doxorubicin 17-20 caspase 3 Homo sapiens 126-135 27286189-2 2016 DEVD-S-DOX, DOX linked to a peptide moiety (DEVD), is a prodrug that is cleaved into free DOX by caspase-3 upon apoptosis. Doxorubicin 7-10 caspase 3 Homo sapiens 97-106 27286189-2 2016 DEVD-S-DOX, DOX linked to a peptide moiety (DEVD), is a prodrug that is cleaved into free DOX by caspase-3 upon apoptosis. Doxorubicin 12-15 caspase 3 Homo sapiens 97-106 27286189-3 2016 DEVD-S-DOX has no therapeutic efficacy, but it changes into free DOX with the expression of caspase-3. Doxorubicin 7-10 caspase 3 Homo sapiens 92-101 27286189-4 2016 With the accumulation of the composite NPs in the tumor tissue by the enhanced permeation and retention (EPR) effect, a small exposure of DOX in the tumor cells initiated apoptosis in a localized area of the tumor tissue, which induced caspase-3 activation. Doxorubicin 138-141 caspase 3 Homo sapiens 236-245 27286189-5 2016 Cleavage of DEVD-S-DOX into free DOX by caspase-3 continued with repetitive activation of caspase-3 and cleavage of DEVD-S-DOX at the tumor site. Doxorubicin 19-22 caspase 3 Homo sapiens 40-49 27286189-5 2016 Cleavage of DEVD-S-DOX into free DOX by caspase-3 continued with repetitive activation of caspase-3 and cleavage of DEVD-S-DOX at the tumor site. Doxorubicin 19-22 caspase 3 Homo sapiens 90-99 27278553-6 2016 Results also indicated that Dox induced apoptosis by upregulating Bax, caspase-8 and caspase-3 and downregulation of Bcl-2 protein expression. Doxorubicin 28-31 caspase 3 Homo sapiens 85-94 27491234-10 2016 ICT and DOX could cause either early or late stage apoptosis, down-regulate Bcl-2 gene expression, and up-regulate gene expressions of Caspase-3 and p21 respectively (P < 0.05). Doxorubicin 8-11 caspase 3 Homo sapiens 135-144 27491234-12 2016 CONCLUSION: CT combined DOX had additive or synergistic inhibition effect for the proliferation of osteosarcoma MG-63 cells, which might be related with regulating gene expressions of bcl-2, caspase-3, and p21. Doxorubicin 24-27 caspase 3 Homo sapiens 191-200 26525975-7 2016 The intracellular production of reactive oxygen species, mitochondrial membrane depolarization, apoptosis level, procaspase 9 and PARP activities, and caspase 3 and caspase 9 activities were higher in the DOX and MEL groups than in the control. Doxorubicin 205-208 caspase 3 Homo sapiens 151-160 26987078-7 2016 In order to confirm apoptosis in the doxorubicin-treated cells, the activities of caspases-3/7 and -9 were determined using a TBE assay. Doxorubicin 37-48 caspase 3 Homo sapiens 82-101 26987078-8 2016 The results indicated that the activities of caspases-3/7 and -9 were significantly elevated in the doxorubicin-treated MDA-MB-231 cells by 571 and 645%, respectively, and in the MCF 7 cells by 471 and 345%, respectively, compared with the control cells. Doxorubicin 100-111 caspase 3 Homo sapiens 45-64 26505786-6 2016 Treatment with 5-FU or DOX in combination with curcumin induced apoptosis by inhibiting Bcl-2 and increasing Bax, caspase-3, and poly-ADP ribose polymerase (PARP) in NT8e cells. Doxorubicin 23-26 caspase 3 Homo sapiens 114-123 26757339-6 2016 We also found that knockdown of cystatin C reduced adriamycin-induced caspase-3 activation. Doxorubicin 51-61 caspase 3 Homo sapiens 70-79 26590797-9 2016 Moreover, IAZP augmented the doxorubicin-induced degradation of p21, activation of p53, CDK2, caspase 3/7 and phosphorylation of Rb protein. Doxorubicin 29-40 caspase 3 Homo sapiens 94-103 26426519-7 2016 Furthermore, the formation of cleaved caspase-3 protein in the group given DOX with taurine was lower than that in the group treated with DOX alone. Doxorubicin 75-78 caspase 3 Homo sapiens 38-47 26426519-7 2016 Furthermore, the formation of cleaved caspase-3 protein in the group given DOX with taurine was lower than that in the group treated with DOX alone. Doxorubicin 138-141 caspase 3 Homo sapiens 38-47 26520467-6 2016 In solid tumor cell lines, the DOX-TRF conjugate induced changes in cellular morphology, mitochondrial membrane potential and caspases-3 and -9 activities. Doxorubicin 31-34 caspase 3 Homo sapiens 126-143 26770398-7 2015 We found that combination treatment of YM155 and DOX in DOX resistant cells (MG63/DOX) could significantly inhibited cell proliferation and colony formation, induce cell apoptosis and promoted caspase-3, -8, and -9 activity in vitro, and promoted tumor regression in established OS xenograft models. Doxorubicin 49-52 caspase 3 Homo sapiens 193-214 26645568-9 2015 In contrast, 48 hr treatment with Dox alone dramatically increased Caspase-3 activity, resulting in cell death. Doxorubicin 34-37 caspase 3 Homo sapiens 67-76 26548747-10 2015 Microscopic examination of tumour tissues showed a significant increase in active (cleaved) caspase-3 expression in PEITC and/or Dox treated groups. Doxorubicin 129-132 caspase 3 Homo sapiens 92-101 26770398-7 2015 We found that combination treatment of YM155 and DOX in DOX resistant cells (MG63/DOX) could significantly inhibited cell proliferation and colony formation, induce cell apoptosis and promoted caspase-3, -8, and -9 activity in vitro, and promoted tumor regression in established OS xenograft models. Doxorubicin 56-59 caspase 3 Homo sapiens 193-214 26770398-7 2015 We found that combination treatment of YM155 and DOX in DOX resistant cells (MG63/DOX) could significantly inhibited cell proliferation and colony formation, induce cell apoptosis and promoted caspase-3, -8, and -9 activity in vitro, and promoted tumor regression in established OS xenograft models. Doxorubicin 56-59 caspase 3 Homo sapiens 193-214 26252906-7 2015 Supporting this finding, the activity and expression of caspase-3 were observed to be enhanced in the U2-OS cells following treatment with either PEITC or ADM, or a combination of the two. Doxorubicin 155-158 caspase 3 Homo sapiens 56-65 26340617-8 2015 Interestingly, we found that Pi strongly increases doxorubicin-induced cytotoxicity in MDA-MB-231 cells by apoptosis induction, as revealed by a marked increase of sub-G1 population, Bcl-2 downregulation, caspase-3 activation and PARP cleavage. Doxorubicin 51-62 caspase 3 Homo sapiens 205-214 26263187-0 2015 Optimization of a Stable Linker Involved DEVD Peptide-Doxorubicin Conjugate That Is Activated upon Radiation-Induced Caspase-3-Mediated Apoptosis. Doxorubicin 54-65 caspase 3 Homo sapiens 117-126 26263187-1 2015 The current study demonstrates the process of selecting an optimal structure for a caspase-3-cleavable doxorubicin prodrug that could be synthesized by simple chemistry in high yields. Doxorubicin 103-114 caspase 3 Homo sapiens 83-92 25997894-7 2015 H9c2 cardiomyoblasts cultured in the galactose-modified media showed lower DOX-induced activation of the apoptotic pathway, measured by decreased caspase-3 and -9 activation, and lower p53 expression, although ultimately loss of cells was not prevented. Doxorubicin 75-78 caspase 3 Homo sapiens 146-162 24998637-6 2014 Subsequently, we conducted a more accurate evaluation of DOX-TRF-trigged cell death by using DNA ladder assay, measuring the activation of caspase-3, -8 and -9 and changes in poly-ADP ribose polymerase (PARP) activity. Doxorubicin 57-60 caspase 3 Homo sapiens 139-159 25895636-8 2015 However, we observed that, truncated Apaf-1 molecules can activate caspase-3/7 upon the induction of apoptosis via doxorubicin. Doxorubicin 115-126 caspase 3 Homo sapiens 67-76 25760224-11 2015 Furthermore, the inhibition of FoxM1 by thiostrepton enhanced doxorubicin-induced apoptosis, possibly through a caspase-3-dependent pathway, and increased the accumulation of intracellular doxorubicin, possibly through downregulating the expression of glutathione S-transferase pi. Doxorubicin 62-73 caspase 3 Homo sapiens 112-121 25775367-5 2015 In galectin-3 overexpressed PC-3 human prostate carcinoma cells, P-(G3-C12)-DOX-Fu surprisingly exhibited comparable cytotoxicity to free DOX at high concentration by increasing cell internalization and exerting synergistic genotoxic effects of cell cycle arrest, caspase-3 activation, and DNA damage. Doxorubicin 76-79 caspase 3 Homo sapiens 264-273 26137410-9 2015 Monocyte mediated resistance to DOX killing was associated with decreased Caspase-3 activity and increased anti-apoptotic heat shock protein-27 (Hsp27) expression. Doxorubicin 32-35 caspase 3 Homo sapiens 74-83 25561091-8 2015 Moreover, a significant increase in caspase-3 activity, DNA fragmentation, and morphological changes in ovarian cells were observed predominantly in new DOX analogues. Doxorubicin 153-156 caspase 3 Homo sapiens 36-45 25294909-11 2014 When combined with doxorubicin, 34.5ENVE killed synergistically with a significant increase in caspase-3/7 activation, and an increase in sub-G1 population of cells. Doxorubicin 19-30 caspase 3 Homo sapiens 95-104 25566959-4 2015 A doxorubicin-responsive green fluorescent protein (GFP) reporter assay indicated that resistance in BFTC-905-DOXO-II was not due to increased drug efflux pump activity, whereas caspase-3/7 activation was indeed diminished. Doxorubicin 2-13 caspase 3 Homo sapiens 178-187 26261798-7 2015 Moreover, doxorubicin-induced caspase-3 activity was attenuated in the presence of cAMP-increasing agents. Doxorubicin 10-21 caspase 3 Homo sapiens 30-39 25605018-5 2015 Furthermore, the caspase-9 and caspase-3 cascade was activated by the functional DOX nanoparticles through upregulation of the pro-apoptotic proteins Bax and Bid and suppression of the antiapoptotic protein Bcl-2, thereby enhancing apoptosis by acting on the mitochondrial signaling pathways. Doxorubicin 81-84 caspase 3 Homo sapiens 31-40 25658463-9 2015 Treatment of wild-type TP53 neuroblastoma cell lines with both GSK2830371 and either doxorubicin or carboplatin resulted in enhanced cell death, mediated through caspase 3/7 induction, as compared to either agent alone. Doxorubicin 85-96 caspase 3 Homo sapiens 162-171 24239681-9 2014 Treatment of HeLa cells with DOX-loaded L-hMS elicited a sufficient degree of biological efficacy of DOX, as confirmed in the DOX-induced apoptotic behaviors, including stimulation in caspase-3 expression, and was even more effective than the direct DOX treatment. Doxorubicin 29-32 caspase 3 Homo sapiens 184-193 24239681-9 2014 Treatment of HeLa cells with DOX-loaded L-hMS elicited a sufficient degree of biological efficacy of DOX, as confirmed in the DOX-induced apoptotic behaviors, including stimulation in caspase-3 expression, and was even more effective than the direct DOX treatment. Doxorubicin 101-104 caspase 3 Homo sapiens 184-193 24239681-9 2014 Treatment of HeLa cells with DOX-loaded L-hMS elicited a sufficient degree of biological efficacy of DOX, as confirmed in the DOX-induced apoptotic behaviors, including stimulation in caspase-3 expression, and was even more effective than the direct DOX treatment. Doxorubicin 101-104 caspase 3 Homo sapiens 184-193 24239681-9 2014 Treatment of HeLa cells with DOX-loaded L-hMS elicited a sufficient degree of biological efficacy of DOX, as confirmed in the DOX-induced apoptotic behaviors, including stimulation in caspase-3 expression, and was even more effective than the direct DOX treatment. Doxorubicin 101-104 caspase 3 Homo sapiens 184-193 23965518-5 2013 ERK1/2 related p53 activation, but not reactive oxygen species, was responsible for Doxorubicin induced caspase-3 cleavage. Doxorubicin 84-95 caspase 3 Homo sapiens 104-113 23956031-6 2014 this study indicates that FA modified MNPs enhances the DOX-induced apoptosis in both of the human ovarian cancer cell lines with sharp decreases in the levels of bcl-2 and surviving, and increased expression of caspase-3. Doxorubicin 56-59 caspase 3 Homo sapiens 212-221 24021537-7 2013 Also, didox combination significantly increase the caspase-3 level compared to DOX treatment alone. Doxorubicin 79-82 caspase 3 Homo sapiens 51-60 24525822-3 2014 Co-treatment with VOR and DOX at marginal doses led to the induction of apoptosis through caspase-3 activation, poly (ADP-ribose) polymerase cleavage and DNA micronuclei. Doxorubicin 26-29 caspase 3 Homo sapiens 90-99 26351207-4 2014 Results found that cellular viability was downregulated while caspase 3 activity and expression were promoted in osteosarcoma cells following treatment with various doses of doxorubicin for 24, 48, and 72 h, and the effects showed a dose- and time-dependent manner. Doxorubicin 174-185 caspase 3 Homo sapiens 62-71 23647679-5 2013 Significantly lower caspase-3 and caspase-8 activity was also observed in the response of these cells to CO1 compared with DOX treatment. Doxorubicin 123-126 caspase 3 Homo sapiens 20-29 24064045-5 2013 Here, we demonstrated that dox inhibited cell viability and induced DNA fragmentation and activation of caspases-3, -7 and -9 in the breast cancer-derived cell lines MCF7 and MDA-MB-231, regardless of different p53 status. Doxorubicin 27-30 caspase 3 Homo sapiens 104-125 23881906-1 2013 Drug Design: An (18)F-labeled caspase-3-sensitive nanoaggregation positron emission tomography tracer was prepared and evaluated for imaging the caspase-3 activity in doxorubicin-treated tumor xenografts. Doxorubicin 167-178 caspase 3 Homo sapiens 30-39 23881906-1 2013 Drug Design: An (18)F-labeled caspase-3-sensitive nanoaggregation positron emission tomography tracer was prepared and evaluated for imaging the caspase-3 activity in doxorubicin-treated tumor xenografts. Doxorubicin 167-178 caspase 3 Homo sapiens 145-154 22674530-7 2013 Interestingly, we found that Pi strongly enhances doxorubicin-induced cytotoxicity in U2OS, and not in Saos and MG63 cells, by apoptosis induction, as revealed by a marked increase of sub-G1 population, Bcl-2 downregulation, caspase-3 activation, and PARP cleavage. Doxorubicin 50-61 caspase 3 Homo sapiens 225-234 23818927-9 2013 Conversely, tyrosine phosphatase inhibitor pervanadate reversed STAT3 inactivation and also PARP cleavage and caspase-3 activation induced by combined treatment of doxorubicin and decursin in U266 cells. Doxorubicin 164-175 caspase 3 Homo sapiens 110-119 22569233-7 2012 The curcumin-DOX combination also suppressed activation of caspase-3, -8, and -9 compared to DOX alone. Doxorubicin 13-16 caspase 3 Homo sapiens 59-80 22770903-7 2012 Moreover, juxtapositioning of Apaf-1 monomer and apoptosome formation occur about 5h earlier than the appearance of significant caspase3/7 activity upon induction of apoptosis by doxorubicin. Doxorubicin 179-190 caspase 3 Homo sapiens 128-136 22581584-6 2012 Conversely, RNA interference-mediated silencing of endogenous ADAM10 potentiated doxorubicin-induced apoptosis in HepG2 and Hep3B cells, which was coupled with increased cleavage of caspase-3 and decreased expression of Mcl-1. Doxorubicin 81-92 caspase 3 Homo sapiens 182-191 23200181-6 2013 Furthermore, the expression of p53, Fas, Bax and activated caspase-3 protein was significantly upregulated in cells treated with HMME-SDT and DOX, whereas Bcl-2 protein was downregulated. Doxorubicin 142-145 caspase 3 Homo sapiens 59-68 22895638-7 2012 DOX/SPIO enhanced caspase-3 activity by twofold compared with free DOX base. Doxorubicin 0-3 caspase 3 Homo sapiens 18-27 21947872-9 2012 Dicoumarol treatment alone potentiated Dox-induced caspase-3 activity. Doxorubicin 39-42 caspase 3 Homo sapiens 51-60 22323498-10 2012 Furthermore, inhibition of JAK-STAT signaling significantly reduced doxorubicin-induced caspase 3 activation and desensitized HeLa cells to doxorubicin cytotoxicity. Doxorubicin 68-79 caspase 3 Homo sapiens 88-97 22198116-0 2012 Anthraquinone antitumour agents, doxorubicin, pirarubicin and benzoperimidine BP1, trigger caspase-3/caspase-8-dependent apoptosis of leukaemia sensitive HL60 and resistant HL60/VINC and HL60/DOX cells. Doxorubicin 33-44 caspase 3 Homo sapiens 91-100 22781804-12 2012 (3) After treated with ADM for 12 and 24 h, the activities of caspase-3 in PTEN-transfected K562/ADM cells increased compared with those in pGFP-transfected K562/ADM cells \[(2.27 +- 0.13) vs (1.19 +- 0.14)\] at 12h, \[(3.15 +- 0.08) vs (1.48 +- 0.05)\] at 24 h (P < 0.05). Doxorubicin 23-26 caspase 3 Homo sapiens 62-71 22198116-0 2012 Anthraquinone antitumour agents, doxorubicin, pirarubicin and benzoperimidine BP1, trigger caspase-3/caspase-8-dependent apoptosis of leukaemia sensitive HL60 and resistant HL60/VINC and HL60/DOX cells. Doxorubicin 192-195 caspase 3 Homo sapiens 91-100 23028696-5 2012 Decreases in doxorubicin fluorescence lifetimes were found to be concurrent with increases in phosphorylation of H2AX (an immediate signal of DNA double-strand breakage), but preceded activation of caspase-3 (a late signature of apoptosis) by more than 150 minutes. Doxorubicin 13-24 caspase 3 Homo sapiens 198-207 22375097-5 2012 Cancer cells with higher levels of full-length survivin and survivin-2B expression, exhibited reduced caspase-3 activation following doxorubicin treatment and radiation. Doxorubicin 133-144 caspase 3 Homo sapiens 102-111 22305266-10 2012 Likewise, down-regulation of p65 expression enhanced the cytotoxic effect of DOX, due to a significant decrease of mRNA levels of anti-apoptotic genes, such as the cellular inhibitor of apoptosis-1 (c-IAP1), and the long isoform of B cell leukemia/lymphoma-2 (Bcl-2), leading to efficient induction of caspase-3 cleavage in the cells. Doxorubicin 77-80 caspase 3 Homo sapiens 302-311 22305266-11 2012 More, we present evidence that over-expression of p53 or p53/p65 in the PANC1 cells were more sensitive to DOX treatment, correlated with activation of caspase-3 and clear elevation of nuclear p21 level. Doxorubicin 107-110 caspase 3 Homo sapiens 152-161 21940668-3 2012 We hypothesized that doxorubicin causes skeletal muscle catabolism through ROS, causing upregulation of E3 ubiquitin ligases and caspase-3. Doxorubicin 21-32 caspase 3 Homo sapiens 129-138 20461381-9 2011 The caspase-3/7 activity was increased with doxorubicin and PCI-24781 treatment in these cells. Doxorubicin 44-55 caspase 3 Homo sapiens 4-13 21865289-6 2011 Along with this, apoptosis was induced by DOX as determined by the dissipation of mitochondrial membrane potential (Deltapsi), cytochrome c release, Bax translocation, and caspase-3 activation. Doxorubicin 42-45 caspase 3 Homo sapiens 172-181 21818667-8 2011 Finally, molecular analysis of apoptosis by western blotting proved activation of caspase 3 followed by poly ADP ribose polymerase (PARP) cleavage more efficiently in Baneh than in Dox treated cancer cells. Doxorubicin 181-184 caspase 3 Homo sapiens 82-91 21078300-5 2010 The reduction in endogenous PIH1D1 by siRNA enhanced apoptosis and caspase-3 activation induced by doxorubicin in U2OS cells. Doxorubicin 99-110 caspase 3 Homo sapiens 67-76 20405239-7 2010 Furthermore, doxorubicin increased the activation of caspase-3 and decreased the phosphorylation of Bad, while simultaneous PACAP treatment reduced the caspase-3 activation and increased the level of phospho-Bad. Doxorubicin 13-24 caspase 3 Homo sapiens 53-62 20884855-3 2010 Cotreatment with sildenafil enhanced DOX-induced apoptosis in PC-3 and DU145 prostate cancer cells, which was mediated by enhanced generation of reactive oxygen species, up-regulation of caspase-3 and caspase-9 activities, reduced expression of Bcl-xL, and phosphorylation of Bad. Doxorubicin 37-40 caspase 3 Homo sapiens 187-196 20682173-8 2010 Importantly, we found that the downregulation of survivin by pSUPER-sh could enhance the anticancer effects of chemotherapies such as etoposide, cisplatin and doxorubicin through decreasing mitochondrial membrane potentials and increasing caspase-3 activity. Doxorubicin 159-170 caspase 3 Homo sapiens 239-248 20512627-6 2010 Combined Dox + DMPS treatment-induced apoptosis was accompanied by the activation of caspase-8 and caspase-3 as well as PARP cleavage. Doxorubicin 9-12 caspase 3 Homo sapiens 99-108 20512627-8 2010 Pretreatment with z-VAD-fmk markedly prevented caspase-3 activation and moderately suppressed apoptosis, suggesting that Dox + DMPS-induced apoptosis is somewhat (not completely) dependent on caspase. Doxorubicin 121-124 caspase 3 Homo sapiens 47-56 20512627-10 2010 The ROS scavenger NAC efficiently suppressed not only ROS generation, but also caspase-3-mediated PARP cleavage, apoptosis, and release of cytochrome c and AIF, indicating a role of ROS in combined Dox + DMPS treatment-induced apoptotic death signaling. Doxorubicin 198-201 caspase 3 Homo sapiens 79-88 20663232-7 2010 Moreover, TRAIL inhibited P-gp efflux function via caspase-3-dependent degradation of P-gp as well as DNA-PKcs and subsequently sensitized MDR cells to MDR-related drugs such as vinblastine and doxorubicin. Doxorubicin 194-205 caspase 3 Homo sapiens 51-60 20528452-7 2010 Phage-Doxil-induced tumor cell killing and apoptosis were confirmed by CellTiter-Blue Assay and caspase-3/CPP32 fluorometric assay. Doxorubicin 6-11 caspase 3 Homo sapiens 96-105 20528452-7 2010 Phage-Doxil-induced tumor cell killing and apoptosis were confirmed by CellTiter-Blue Assay and caspase-3/CPP32 fluorometric assay. Doxorubicin 6-11 caspase 3 Homo sapiens 106-111 19426282-6 2009 Conspicuously, DOX-treated platelets displayed apoptotic features such as caspase-3 activation, reduced mitochondrial transmembrane potential, and phosphatidylserine exposure. Doxorubicin 15-18 caspase 3 Homo sapiens 74-83 20508289-5 2010 Furthermore, QA3 triggered and increased adriamycin-induced K562/A02 cell apoptosis as evidenced by Annexin V-FITC plus PI staining.Western blot analysis showed that the levels of cleaved caspase-9 and cleaved caspase-3 proteins increased, and similarly, the levels of procaspase-9 and procaspase-3 decreased after QA3 treatment. Doxorubicin 41-51 caspase 3 Homo sapiens 286-298 21364639-5 2010 alphaA-crystallin inhibited doxorubicin-mediated activation of human procaspase-3 in CHO cells and it activated the PI3K/Akt cell survival pathway by promoting the phosphorylation of PDK1, Akt and phosphatase tensin homologue in HeLa cells. Doxorubicin 28-39 caspase 3 Homo sapiens 69-81 20193325-4 2009 The effect of bortezomib and adriamycin on the expression levels of caspase-3, caspase-8 and PARP were measured by Nestern blot. Doxorubicin 29-39 caspase 3 Homo sapiens 68-77 19902123-6 2009 Transmission electron microscopy and the measurements of caspase-3 levels in treated cells revealed that the co-treatment of cells with ADM and TMPyP followed by light irradiation directed the cell death towards necrosis and abrogated the apoptotic cell death pathway, which was exhibited in cells treated with ADM in absence and in presence of photoirradiation. Doxorubicin 136-139 caspase 3 Homo sapiens 57-66 19426282-9 2009 These in vitro results were further confirmed by an in vivo animal model, where administration of DOX induced a platelet count decrease, ROS generation, caspase-3 activation, protein thiol depletion, and damaged platelet integrity. Doxorubicin 98-101 caspase 3 Homo sapiens 153-162 19190340-12 2009 When WT1 expression was prohibited, doxorubicin caused a marked increase in caspase-3 activation. Doxorubicin 36-47 caspase 3 Homo sapiens 76-85 18758960-4 2008 Moreover, let-7a was over-expressed while caspase-3 was down-regulated in A10A cells, a doxorubicin-resistant A431 subline. Doxorubicin 88-99 caspase 3 Homo sapiens 42-51 19082486-4 2009 Doxorubicin induced dose-dependent G2/M and/or G1/S cell cycle arrest, followed by grade- and dose-dependent reduction in the amount of the cytosolic trimeric form of FasL, activation of Caspase-8, Caspase-9, Caspase-3, cleavage of PARP, Lamin A/C, Bcl-XL/S and interestingly Hsp90, and finally cell death. Doxorubicin 0-11 caspase 3 Homo sapiens 209-218 18758960-6 2008 On the other hand, down-regulation of let-7a by the anti-let-7a inhibitor increased the doxorubicin-induced apoptosis in A431 parent cells, A10A cells and HepG2 cells while the increase was suppressed by caspase-3 inhibitor. Doxorubicin 88-99 caspase 3 Homo sapiens 204-213 18422996-10 2008 In RS4:11 cells, combining G3139 with doxorubicin (ADR) increased active caspase 3 and TUNEL staining compared to ADR alone, indicating greater apoptosis, and G3139 increased S-phase progression. Doxorubicin 38-49 caspase 3 Homo sapiens 73-82 18852119-7 2008 Furthermore, AF1q enhanced the mitochondrial membrane depolarization, mitochondrial cytochrome c release, and activation of caspase-9 and caspase-3 on doxorubicin treatment. Doxorubicin 151-162 caspase 3 Homo sapiens 138-147 18278454-6 2008 The activation of Caspase-3 and PARP induced by doxorubicin was tested by Western blotting. Doxorubicin 48-59 caspase 3 Homo sapiens 18-27 17996985-6 2008 Memantine at low micromolar concentrations also attenuated salsolinol- and doxorubicin-induced LDH release and DNA fragmentation, but only in the case of salsolinol was this effect accompanied by a decrease in caspase-3 activity. Doxorubicin 75-86 caspase 3 Homo sapiens 210-219 17935137-9 2008 Furthermore, wortmannin promoted etoposide and doxorubicin induced caspase-3, caspase-9 activation and poly ADP-ribose polymerase cleavage. Doxorubicin 47-58 caspase 3 Homo sapiens 67-76 17542780-5 2007 Further studies showed that morphine inhibited ROS (reactive oxygen species) generation, and prevented DOX-mediated caspase-3 activation, cytochrome c release and changes of Bax and Bcl-2 protein expression. Doxorubicin 103-106 caspase 3 Homo sapiens 116-125 17959036-7 2007 IFNalpha markedly upregulated p53, Bax, Mdm2, and p21, downregulated Bcl-2, and activated caspase-3 and PARP cleavage in response to doxorubicin in U2OS cells. Doxorubicin 133-144 caspase 3 Homo sapiens 90-99 18164246-4 2008 Doxorubicin induced increases in both annexin V labelling and caspase-3 activity and decreases in cell volume. Doxorubicin 0-11 caspase 3 Homo sapiens 62-71 17965021-7 2007 Consistent with this result, inhibition of the LPA(2) receptor expression increases Siva-1 protein levels and augments adriamycin-induced caspase-3 cleavage and apoptosis. Doxorubicin 119-129 caspase 3 Homo sapiens 138-147 17922852-8 2007 Furthermore, the combination of doxorubicin and lexatumumab significantly enhanced caspase 8 activity, Bid cleavage, Bcl-xL decrease, release of cytochrome c, and caspase 9 and caspase 3 activity, and induced synergistic apoptosis. Doxorubicin 32-43 caspase 3 Homo sapiens 177-186 17706502-6 2007 RESULTS: Wild-type and Dox-R cells had maximal total caspase 3 expression after incubation with EGF (5 ng/mL) for 3 and 5 days, respectively, and a corresponding increase in DNA transcription. Doxorubicin 23-26 caspase 3 Homo sapiens 53-62 18246814-5 2007 The activation of caspase-3 and PARP induced by doxorubicin was tested by Western blotting. Doxorubicin 48-59 caspase 3 Homo sapiens 18-27 17706502-10 2007 CONCLUSION: Epidermal growth factor upregulates the expression and transcription of total caspase 3 in WT and Dox-R cells in a concentration- and time-dependent manner. Doxorubicin 110-113 caspase 3 Homo sapiens 90-99 16937080-8 2007 Furthermore, it was found that DDB promoted doxorubicin-induced apoptosis of Bel(7402) cells through enhanced caspase-3 activation. Doxorubicin 44-55 caspase 3 Homo sapiens 110-119 17031387-7 2006 The antitumour/proapoptotic effects of doxorubicin and bleomycin were assessed by cell proliferation and caspase-3 activity assay. Doxorubicin 39-50 caspase 3 Homo sapiens 105-114 17097318-8 2007 Furthermore, both TUNEL and pro-caspase-3 expression assay showed a significant increase in apoptosis after combined treatment with adriamycin and siRNA targeting IGF1R. Doxorubicin 132-142 caspase 3 Homo sapiens 18-41 17013758-0 2006 Caspase-3 mediated feedback activation of apical caspases in doxorubicin and TNF-alpha induced apoptosis. Doxorubicin 61-72 caspase 3 Homo sapiens 0-9 17013758-3 2006 We have previously shown that caspase-3 reconstitution significantly sensitized MCF-7 cells to doxorubicin and etoposide. Doxorubicin 95-106 caspase 3 Homo sapiens 30-39 17013758-4 2006 In contrast to the well established role of caspase-3 as an effector caspase, the focus of this study is to delineate caspase-3 induced feedback activation of the apical caspases-2, -8, -9 and -10A in doxorubicin and TNF-alpha induced apoptosis. Doxorubicin 201-212 caspase 3 Homo sapiens 118-127 17013758-6 2006 When apoptosis is induced by doxorubicin or TNF-alpha in an intact cell model, cleavage of caspases-8 and -9, but not caspase-2, was markedly enhanced by caspase-3. Doxorubicin 29-40 caspase 3 Homo sapiens 154-163 16545138-1 2006 BACKGROUND: CD40L was found to reduce doxorubicin-induced apoptosis in non Hodgkin"s lymphoma cell lines through caspase-3 dependent mechanism. Doxorubicin 38-49 caspase 3 Homo sapiens 113-122 16962673-3 2006 In this report, using Hoechst reagent staining, reactive oxygen species production and caspase-3 activity measurement, we determined that both camptothecin and doxorubicin induced apoptosis in human thyroid carcinoma cells (FTC-133). Doxorubicin 160-171 caspase 3 Homo sapiens 87-96 16909308-0 2006 Requirement for pre-existing of p21 to prevent doxorubicin-induced apoptosis through inhibition of caspase-3 activation. Doxorubicin 47-58 caspase 3 Homo sapiens 99-108 16909308-4 2006 Here we report that pre-existing p21 can associate with pro-caspase-3 and inhibit caspase-3 activation in the cells, which was at least in part responsible for enhancing survival of DOX-treated cells. Doxorubicin 182-185 caspase 3 Homo sapiens 56-69 16909308-4 2006 Here we report that pre-existing p21 can associate with pro-caspase-3 and inhibit caspase-3 activation in the cells, which was at least in part responsible for enhancing survival of DOX-treated cells. Doxorubicin 182-185 caspase 3 Homo sapiens 60-69 16843435-4 2006 Furthermore, blocking phosphatidylinositol-3-kinase/Akt signaling significantly increased doxorubicin-induced caspase-3 activity and cell death, indicating that Akt is a survival factor in this system. Doxorubicin 90-101 caspase 3 Homo sapiens 110-119 17054846-11 2006 After the treatment of adriamycin and mitomycin, the expression of XIAP was down-regulated dose-dependently, however, being weaker in the T24 cells than in the RT4 cells; and caspase-3 precursor cleavage was enhanced, however, being weaker in the T24 cells too. Doxorubicin 23-33 caspase 3 Homo sapiens 175-184 16108013-9 2006 Furthermore, both TUNEL and pro-caspase3 expression assay showed a significant increase in apoptosis after combined treatment with adriamycin and siRNA targeting survivin. Doxorubicin 131-141 caspase 3 Homo sapiens 32-40 15868924-2 2005 Doxorubicin activated caspases 3, 8 and 9 in both HSC-2 and HL-60 cells, but induced internucleosomal DNA fragmentation only in HL-60 cells. Doxorubicin 0-11 caspase 3 Homo sapiens 22-41 16139916-4 2005 FOL-PEG-PEI conjugate complexed with rev-caspase-3 plasmid in an optimized condition gave rise to a great increase in expression and activation of exogenous rev-caspase-3 in KB cells when pretreated with doxorubicin. Doxorubicin 204-215 caspase 3 Homo sapiens 41-50 16139916-4 2005 FOL-PEG-PEI conjugate complexed with rev-caspase-3 plasmid in an optimized condition gave rise to a great increase in expression and activation of exogenous rev-caspase-3 in KB cells when pretreated with doxorubicin. Doxorubicin 204-215 caspase 3 Homo sapiens 161-170 16319532-6 2006 Significant activation of caspase-2 and caspase-3 was only observed in MDA-MB-231 cells treated with doxorubicin but not with WP631, indicating that caspases may be not mandatory for the occurrence of cell death through mitotic catastrophe. Doxorubicin 101-112 caspase 3 Homo sapiens 40-49 16086872-17 2005 Combination treatment of ASODN and ADM gradually enhanced activity of Caspase-3 and cell apoptosis in a concentration-dependent manner, and resulted in caspase-dependent cell death in HepG2/ADM cells. Doxorubicin 35-38 caspase 3 Homo sapiens 70-79 15985719-0 2005 Induction of caspase 3 activity, bcl-2 bax and p65 gene expression modulation in human acute promyelocytic leukemia HL-60 cells by doxorubicin with amifostine. Doxorubicin 131-142 caspase 3 Homo sapiens 13-22 15985719-9 2005 HL-60 cells treated with doxorubicin alone showed about 35-fold increase in caspase 3 activity. Doxorubicin 25-36 caspase 3 Homo sapiens 76-85 15578696-6 2005 Our results suggest that p53-R175H mutation may gain new function in decreasing DOX-induced apoptotic response through suppression of caspase-3 level and its activation. Doxorubicin 80-83 caspase 3 Homo sapiens 134-143 15680309-13 2005 This oxidative DNA damage causes indirect H(2)O(2) generation through PARP and NAD(P)H oxidase activation, leading to the Delta Psi m increase and subsequent caspase-3 activation in DOX-induced apoptosis. Doxorubicin 182-185 caspase 3 Homo sapiens 158-167 15763945-5 2004 Similarly caspase-3 activity was significantly elevated in HCAECs treated with doxorubicin, daunorubicin, and idamycin. Doxorubicin 79-90 caspase 3 Homo sapiens 10-19 15623433-8 2005 After 24 h DOX-treatment, SNAP reduced the increased caspase-3 activity by 63%, and this effect was reversed by treatment with HgCl2. Doxorubicin 11-14 caspase 3 Homo sapiens 53-62 15623433-14 2005 Results showed that formation of nitrosothiol in caspase-3 in DOX-treated cardiomyocytes with SNAP was increased significantly compared with untreated cardiomyocytes. Doxorubicin 62-65 caspase 3 Homo sapiens 49-58 15174092-1 2004 The purpose of this study was to determine whether expression of tissue transglutaminase (TG2) and caspase-3 proteins in drug-resistant breast carcinoma MCF-7/DOX cells would render these cells selectively susceptible to apoptotic stimuli. Doxorubicin 159-162 caspase 3 Homo sapiens 99-108 15174092-7 2004 In summary, these data demonstrate that MCF-7/DOX cells are much more sensitive to apoptotic stimuli than previously thought and that A23187-induced apoptosis may involve some novel, yet unidentified, upstream pathway that leads to the activation of caspase-3 and other downstream events. Doxorubicin 46-49 caspase 3 Homo sapiens 250-259 15233869-5 2004 The induction of apoptosis in MCF-7/dox cells was assessed by established techniques such as TUNEL (terminal deoxynucleotidyl transferase-mediated nick end labelling) staining and caspase-3 assay. Doxorubicin 36-39 caspase 3 Homo sapiens 180-189 15054096-6 2004 In contrast, DOX caused early activation of p53 in tumor cells that was followed by caspase-3 activation and DNA fragmentation. Doxorubicin 13-16 caspase 3 Homo sapiens 84-93 14990581-6 2004 We have investigated the molecular mechanisms involved in executing doxorubicin-induced apoptosis and show caspase-3 activation by both mitochondria-dependent and -independent pathways. Doxorubicin 68-79 caspase 3 Homo sapiens 107-116 14990581-7 2004 Moreover, serine proteases participate in doxorubicin-induced apoptosis partly by contributing to caspase-3 activation. Doxorubicin 42-53 caspase 3 Homo sapiens 98-107 14990581-8 2004 Finally, a complete rescue from doxorubicin-induced apoptosis is obtained only when serine proteases, caspase-3, and mitochondrial activation are inhibited simultaneously. Doxorubicin 32-43 caspase 3 Homo sapiens 102-111 15981920-3 2004 P-(GFLG)-DOX was shown to effect apoptosis-induced tumor cell death as manifested by positive Annexin V-FITC staining, cleavage of procaspase 3 and its physiological substrate, poly(ADP-ribose) polymerase (PARP), and cleavage of procaspase 8. Doxorubicin 9-12 caspase 3 Homo sapiens 131-143 14736733-6 2004 Nonmyocyte-conditioned media also increased protein levels of Bcl-2 but not Bcl-xL and decreased caspase-3 activation induced by DOX. Doxorubicin 129-132 caspase 3 Homo sapiens 97-106 14657946-7 2004 Caspase-3 activity was significantly increased in Karpas-299 and SU-DHL-1 cells treated with doxorubicin, but remained as low as control levels with addition of Boc-D-FMK or DEVD-FMK. Doxorubicin 93-104 caspase 3 Homo sapiens 0-9 14995997-5 2004 In our experiments, doxorubicin induced a dose- and incubation time-dependent and caspase-3-mediated apoptosis of endothelial cells. Doxorubicin 20-31 caspase 3 Homo sapiens 82-91 14657946-11 2004 In conclusion, doxorubicin-induced cell death of ALK-positive ALCL cells involves caspase-3 activation in vitro. Doxorubicin 15-26 caspase 3 Homo sapiens 82-91 11956583-5 2002 The most striking change was the presence of a full-length functional caspase-3 in MCF-7/DOX cells that was missing in the parental MCF-7/WT cells due to a deletion mutation in the caspase-3 gene. Doxorubicin 89-92 caspase 3 Homo sapiens 70-79 12899928-4 2003 Furthermore, DOX increased the intracellular hydrogen peroxide and superoxide levels, followed by mitochondrial membrane depolarization, cytochrome c release, caspase-3 activation, prior to DNA laddering in Saos-2 cells. Doxorubicin 13-16 caspase 3 Homo sapiens 159-168 12899928-6 2003 The role of ROS in DOX induced cell death was confirmed by the suppression effect of catalase on DOX induced ROS formation, mitochondrial cytochrome c release, procaspase-3 cleavage, and apoptosis in Saos-2 cells. Doxorubicin 19-22 caspase 3 Homo sapiens 160-172 12743603-8 2003 The pan-caspase inhibitor (Q-VD-OPH) greatly reduced doxorubicin-induced caspase-3 activation but did not protect cells against drug toxicity. Doxorubicin 53-64 caspase 3 Homo sapiens 73-82 15557793-5 2004 However, U0126 rather enhanced the doxorubicin-induced activation of caspase-3 and poly ADP-ribose polymerase (PARP), and U0126 itself activated caspase-3 and PARP. Doxorubicin 35-46 caspase 3 Homo sapiens 69-78 15557793-6 2004 Interestingly, JNKI-1 inhibited the doxorubicin-induced activation of caspase-3 and PARP. Doxorubicin 36-47 caspase 3 Homo sapiens 70-79 14567645-8 2003 The specific caspase-3 activity in A549 cells treated with nimesulide (40 microg/ml) and doxorubicin (0.25 microg/ml) in combination was 3 and 5 times higher than doxorubicin and nimesulide, respectively. Doxorubicin 89-100 caspase 3 Homo sapiens 13-22 14567645-8 2003 The specific caspase-3 activity in A549 cells treated with nimesulide (40 microg/ml) and doxorubicin (0.25 microg/ml) in combination was 3 and 5 times higher than doxorubicin and nimesulide, respectively. Doxorubicin 163-174 caspase 3 Homo sapiens 13-22 12483536-9 2002 The sensitivity of caspase-3-deficient breast cancer (MCF-7) cells to undergo apoptosis in response to doxorubicin and other apoptotic stimuli could be augmented by reconstituting caspase-3 expression. Doxorubicin 103-114 caspase 3 Homo sapiens 19-28 12483536-9 2002 The sensitivity of caspase-3-deficient breast cancer (MCF-7) cells to undergo apoptosis in response to doxorubicin and other apoptotic stimuli could be augmented by reconstituting caspase-3 expression. Doxorubicin 103-114 caspase 3 Homo sapiens 180-189 12203125-4 2002 Dox induced caspase-3, -7, -8 and -9 and Bid cleavage in S-type cells and death was blocked by caspase inhibitors but not by oxygen radical scavenger BHA. Doxorubicin 0-3 caspase 3 Homo sapiens 12-36 12140766-4 2002 Moreover, while PR3 is involved in the cleavage of caspase-3, PR3-mediated DOX-induced DNA fragmentation and apoptosis were not prevented by a specific inhibitor of caspase-3. Doxorubicin 75-78 caspase 3 Homo sapiens 51-60 11956583-5 2002 The most striking change was the presence of a full-length functional caspase-3 in MCF-7/DOX cells that was missing in the parental MCF-7/WT cells due to a deletion mutation in the caspase-3 gene. Doxorubicin 89-92 caspase 3 Homo sapiens 181-190 11572767-0 2001 Augmented adriamycin sensitivity in cells transduced with an antisense tumor necrosis factor gene is mediated by caspase-3 downstream from reactive oxygen species. Doxorubicin 10-20 caspase 3 Homo sapiens 113-122 11572767-2 2001 In ADM-resistant pancreatic carcinoma (PANC-1) cells, both the antioxidant N-acetyl-L-cysteine (NAC) and the caspase-3 inhibitor acetyl-L-aspartyl-L-methionyl-L-glutaminyl-L-aspartyl-aldehyde (Ac-DMQD-CHO) prevented ADM-induced cytotoxicity. Doxorubicin 3-6 caspase 3 Homo sapiens 109-118 11509031-4 2001 Western blot analysis of HeLa cells treated with DOX for 12 h revealed that DOX caused proteolytic activation of caspase-3 and zinc inhibited this activation. Doxorubicin 49-52 caspase 3 Homo sapiens 113-122 11509031-4 2001 Western blot analysis of HeLa cells treated with DOX for 12 h revealed that DOX caused proteolytic activation of caspase-3 and zinc inhibited this activation. Doxorubicin 76-79 caspase 3 Homo sapiens 113-122 11509031-7 2001 These results demonstrate that zinc specifically inhibits DOX-induced activation of caspase-3 in HeLa cells, but does not suppress DOX-induced apoptosis or otherwise cell death, thus suggesting DOX-induced caspase-3 activation may not play a major role in overall cell death and/or non-caspase-3 pathways are involved in DOX-induced apoptosis in HeLa cells. Doxorubicin 58-61 caspase 3 Homo sapiens 84-93 11289134-4 2001 Consistent with this, FP enhanced DOX-induced activation of caspase-3, which correlates with apoptosis, in pRb-deficient cells but not in pRb-restored cells. Doxorubicin 34-37 caspase 3 Homo sapiens 60-69 10463600-5 1999 The Ku-protein level and Ku DNA binding activity were decreased after treatment with bleomycin, adriamycin, or vincristine, and the decreases were blocked by the treatment of z-DEVD-fmk, a specific inhibitor of caspase-3, suggesting that loss of Ku DNA binding is, in part, due to a caspase-mediated decrease in Ku protein levels. Doxorubicin 96-106 caspase 3 Homo sapiens 211-220 10912804-1 2000 Doxorubicin induces caspase-3 activation and apoptosis in Jurkat cells but inhibition of this enzyme did not prevent cell death, suggesting that another caspase(s) is critically implicated. Doxorubicin 0-11 caspase 3 Homo sapiens 20-29 11196185-0 2001 Reconstitution of caspase 3 sensitizes MCF-7 breast cancer cells to doxorubicin- and etoposide-induced apoptosis. Doxorubicin 68-79 caspase 3 Homo sapiens 18-27 10766178-10 2000 Activation of caspase-3 after daunorubicin or doxorubicin treatment of either nonactivated or activated lymphocytes was demonstrated by the cleavage of poly(ADP-ribose) polymerase, which was, as apoptosis, inhibited by the peptide benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone. Doxorubicin 46-57 caspase 3 Homo sapiens 14-23 10561081-6 2000 When combined with the chemotherapeutic agent doxorubicin, a known CPP32 activator, a dual effect was observed. Doxorubicin 46-57 caspase 3 Homo sapiens 67-72 10561081-7 2000 Low concentrations of heptachlor (5 microM-10 microM) suppressed doxorubicin-induced CPP32 activity, and high concentrations of heptachlor (80 microM-120 microM) augmented it. Doxorubicin 65-76 caspase 3 Homo sapiens 85-90 10582694-8 1999 Doxorubicin increased caspase-3 activity in two ESFT cell lines, TC-32 and TC-71. Doxorubicin 0-11 caspase 3 Homo sapiens 22-31 10582694-9 1999 Concomitant treatment of the doxorubicin-treated cells with IGF-I reduced caspase-3 activity 8-fold in TC-32 and 4-fold in TC-71. Doxorubicin 29-40 caspase 3 Homo sapiens 74-83 10582694-13 1999 A constitutively activated Akt was stably transfected into ESFT and those cells with high levels of expression demonstrated increased resistance to doxorubicin-induced caspase-3 activation. Doxorubicin 148-159 caspase 3 Homo sapiens 168-177 10080945-2 1999 The present study demonstrates that the cytotoxic drugs cisplatin, doxorubicin and mitomycin C induce the accumulation of the Fas receptor, the FADD adaptor molecule, the procaspases-8, -3 and -2L and the proapoptotic molecule Bax in several human colon cancer cells. Doxorubicin 67-78 caspase 3 Homo sapiens 171-196 10489162-5 1999 Caspase-3 activity was increased only in the SKG-3b cell lysate after treatment with CDDP, ADM, and VP-16 but was not found in the SKG-3a cell lysate. Doxorubicin 91-94 caspase 3 Homo sapiens 0-9 9973225-13 1999 This was evidenced by the fact that chemotherapy agents that synergized with TRAIL (e.g., doxorubicin) themselves caused cleavage of caspase-3 and poly(ADP-ribose) polymerase (PARP), and their toxicity was blocked by the caspase inhibitor Z-Val-Ala-Asp(OMe)-CH2 (ZVAD-fmk). Doxorubicin 90-101 caspase 3 Homo sapiens 133-142 9973225-14 1999 The combination of TRAIL and doxorubicin caused significantly greater caspase-3 and PARP cleavage, and the combined toxicity also was inhibited by ZVAD-fmk. Doxorubicin 29-40 caspase 3 Homo sapiens 70-79 9756937-5 1998 Anticancer drugs such as camptothecin, vinblastine, inostamycin, and adriamycin induced activation of caspase-3(-like) proteases and apoptosis. Doxorubicin 69-79 caspase 3 Homo sapiens 102-117 9766678-6 1998 Mitochondria from cells treated with either Doxo or Bet A induced cleavage of both caspase-8 and caspase-3 in cytosolic extracts. Doxorubicin 44-48 caspase 3 Homo sapiens 97-106 9734474-6 1998 Serum withdrawal and doxorubicin reduced cell viability, increased fragmentation of DNA, increased cellular contents of Bax, and activated caspase 3. Doxorubicin 21-32 caspase 3 Homo sapiens 139-148 9734474-9 1998 Thus, cardiomyocyte apoptosis induced by serum withdrawal and doxorubicin likely results, in part, from the induction of Bax and activation of caspase 3, but IGF I may inhibit cardiomyocyte apoptosis by attenuating Bax induction and caspase 3 activation. Doxorubicin 62-73 caspase 3 Homo sapiens 143-152 9409752-6 1997 We conclude that: (i) DOX-induced apoptosis in human T-leukemia/lymphoma is Fas-independent and (ii) caspase-3 is responsible of DOX-induced nuclear apoptosis but other Z-VAD-sensitive caspases are implicated in cell death. Doxorubicin 129-132 caspase 3 Homo sapiens 101-110 9642215-5 1998 Other cells selected for resistance to doxorubicin or vincristine also exhibited overexpression of Bcl-xL and failed to respond to CDDP and ara-C with activation of caspase-3. Doxorubicin 39-50 caspase 3 Homo sapiens 165-174 9409752-0 1997 Doxorubicin-induced apoptosis in human T-cell leukemia is mediated by caspase-3 activation in a Fas-independent way. Doxorubicin 0-11 caspase 3 Homo sapiens 70-79 33589596-6 2021 Furthermore, activation of caspase 3, not caspase 9, is associated with GSDME cleavage in cisplatin- or doxorubicin-treated renal tubular epithelial cells. Doxorubicin 104-115 caspase 3 Homo sapiens 27-36 34874743-4 2022 Patient-specific doxorubicin-induced cardiotoxicity (DIC) was then characterized using assays of cell viability, activated caspase 3/7, and doxorubicin uptake. Doxorubicin 17-28 caspase 3 Homo sapiens 123-134 34656704-9 2022 Furthermore, AML halted DOX-induced hippocampal apoptosis as evidenced by decreased caspase-3 activity and lower cytochrome c immunoexpression. Doxorubicin 24-27 caspase 3 Homo sapiens 84-93 34126102-3 2021 Deferoxamine decreased the number of dead (detached) cells, the size of SubG1 population, the release of cytochrome c, and the processing of caspase-3 in HCT116 colon carcinoma cells treated with cisplatin of doxorubicin. Doxorubicin 209-220 caspase 3 Homo sapiens 141-150 34233077-8 2021 RESULTS: Both HTR8/SVneo and CTBs underwent caspase 3/7 cleavage following DOX treatment, with HTR8/SVneo cells more sensitive to apoptosis than term CTBs. Doxorubicin 75-78 caspase 3 Homo sapiens 44-55 34369076-7 2021 Furthermore, DOX treatments induced intracellular accumulation of ROS, stimulated the phosphorylation of JNK, and Caspase-3 activation, subsequently. Doxorubicin 13-16 caspase 3 Homo sapiens 114-123 34369076-8 2021 In conclusion, the study suggests that GSDME triggered DOX-induced pyroptosis in the caspase-3 dependent reactions through the ROS/JNK signalling pathway. Doxorubicin 55-58 caspase 3 Homo sapiens 85-94 34343539-10 2021 Of note, doxorubicin induced the expression of myocardial nuclear NF-kappaB-p65 and caspase-3 which were markedly inhibited by trifluoperazine, suggesting that cardioprotection conferred by trifluoperazine involved, at least in part, suppression of NF-kappaB and apoptosis. Doxorubicin 9-20 caspase 3 Homo sapiens 84-93 34237409-10 2021 The Dox@mPH-RA increased the levels of apoptosis markers, caspase 3, 7, Ki-67, and caused the highest DNA fragmentation. Doxorubicin 4-7 caspase 3 Homo sapiens 58-67 35452763-0 2022 Feedback amplification of senolysis using caspase-3-cleavable peptide-doxorubicin conjugate and 2DG. Doxorubicin 70-81 caspase 3 Homo sapiens 42-51 35113358-7 2022 Lupeol individually and in combination with DOX up-regulated the expression of caspase-3. Doxorubicin 44-47 caspase 3 Homo sapiens 79-88 35503006-5 2022 Eventually, the expressions of Caspase 3, 6, 7, and 9 genes in the single treatment with DOX had higher alteration compared to the co-treatment with DOX and apigenin (p < 0.05). Doxorubicin 89-92 caspase 3 Homo sapiens 31-53 35503006-5 2022 Eventually, the expressions of Caspase 3, 6, 7, and 9 genes in the single treatment with DOX had higher alteration compared to the co-treatment with DOX and apigenin (p < 0.05). Doxorubicin 149-152 caspase 3 Homo sapiens 31-53 34319045-16 2021 Dox-loaded ASA inhibited the proliferation of SW480 cells, because the aptamer facilitated the Dox uptake into these cells which caused the cell apoptosis, indicated by the significant decrease in procaspase-3, apoptosis marker protein. Doxorubicin 0-3 caspase 3 Homo sapiens 197-209 34319045-16 2021 Dox-loaded ASA inhibited the proliferation of SW480 cells, because the aptamer facilitated the Dox uptake into these cells which caused the cell apoptosis, indicated by the significant decrease in procaspase-3, apoptosis marker protein. Doxorubicin 95-98 caspase 3 Homo sapiens 197-209 34208283-11 2021 Tariquidar enhanced Dox cytotoxicity by increasing intracellular ROS production leading to caspase-3 mediated apoptosis. Doxorubicin 20-23 caspase 3 Homo sapiens 91-100 34353488-5 2021 With 1-RGD, high-resolution 3D PA images of tumor tissues can be obtained, allowing to report on the activity and distribution of caspase-3 within DOX-treated tumors, which was helpful for early monitoring of tumor response to therapy. Doxorubicin 147-150 caspase 3 Homo sapiens 130-139 35579133-16 2022 On the other hand, enzalutamide may sensitize the cells to doxorubicin through downregulation of the bid/bcl2/mcl1 axis that normally activates the executive caspases, caspase 3/7. Doxorubicin 59-70 caspase 3 Homo sapiens 168-179 35447298-3 2022 Here, we describe a tumoral caspase-3 mediated peptide-doxorubicin conjugates (PDC) switch therapy that adopts two different caspase-3 cleavable PDCs, RGDEVD-DOX (TPD1) and EMC-KGDEVD-DOX (MPD1), for targeting metastatic triple-negative breast cancer (mTNBC). Doxorubicin 55-66 caspase 3 Homo sapiens 28-37 35447298-3 2022 Here, we describe a tumoral caspase-3 mediated peptide-doxorubicin conjugates (PDC) switch therapy that adopts two different caspase-3 cleavable PDCs, RGDEVD-DOX (TPD1) and EMC-KGDEVD-DOX (MPD1), for targeting metastatic triple-negative breast cancer (mTNBC). Doxorubicin 55-66 caspase 3 Homo sapiens 125-134 35395977-4 2022 RESULTS: DOX significantly increased the levels of cleaved caspase-3 and caspase-9, and down-regulated the level of p-MEK in H929 (P<0.05). Doxorubicin 9-12 caspase 3 Homo sapiens 59-68 35453640-7 2022 IL-10 was able to reduce the overexpression of mitochondrial apoptotic proteins caspase-3 as well as Bax, which were upregulated upon Dox treatment. Doxorubicin 134-137 caspase 3 Homo sapiens 80-89 35395977-7 2022 Compared with DOX alone treatment group, the expressions of p-MEK and p-ERK1/2 in DOX+ML-098 combined treatment group were increased, and the levels of cleaved caspase-3,9 in H929 cells were decreased (P<0.05). Doxorubicin 14-17 caspase 3 Homo sapiens 160-169 35395977-7 2022 Compared with DOX alone treatment group, the expressions of p-MEK and p-ERK1/2 in DOX+ML-098 combined treatment group were increased, and the levels of cleaved caspase-3,9 in H929 cells were decreased (P<0.05). Doxorubicin 82-85 caspase 3 Homo sapiens 160-169 35216449-8 2022 Conversely, Dox-induced CD133 expression diminished apoptosis in both trametinib-treated cell lines, coincident with elevated p-AKT, p-BAD, BCL-2, and BCL-xL and decreased activation of BAX and caspases-3 and -9. Doxorubicin 12-15 caspase 3 Homo sapiens 194-211 35327403-5 2022 Indeed, when MDR-overexpressing cancer cells were treated with a combination of BGJ 398 and PTX (or Dox), we observed a significant increase of apoptosis which was evidenced by an increased expression of cleaved forms of PARP, caspase-3, and increased numbers of Annexin V-positive cells, as well. Doxorubicin 100-103 caspase 3 Homo sapiens 227-236 33639139-6 2021 Further, after treated with CD19-PEG-MTN/DOX nanoparticle, pro-apoptotic proteins Bax and Caspase-3 in KOPN 8 and NALM-6 cells were significantly upregulated, but anti-apoptotic proteins Bcl2, MCL-1, HSP 70, and BAG 3 were downregulated, which indicated the activation of the apoptosis pathway by the nanodrug. Doxorubicin 41-44 caspase 3 Homo sapiens 90-99 35057107-9 2022 This combination therapy of dox with cobalt (III) complexes resulted in enhanced apoptosis in A549 cells, as evidenced by elevated caspase 3/7 activity in treated groups. Doxorubicin 28-31 caspase 3 Homo sapiens 131-142 33850567-4 2021 Combined HSYB and DOX treatment significantly decreased the expression levels of BCL-2 in MCF-7 cells, while the expression levels of apoptosis-associated proteins, including cleaved caspase-9, BAX and cleaved caspase-3, were markedly increased. Doxorubicin 18-21 caspase 3 Homo sapiens 210-219 35095524-5 2021 In vitro studies show that cyclic-1a promotes the apoptosis of MCF-7/DOX cells by inducing the cleavages of caspase-3 and PARP. Doxorubicin 69-72 caspase 3 Homo sapiens 108-117 32770328-5 2021 Correspondingly, the analysis of histopathological morphology showed that the morphology and density of tumor tissue in hydrogel/DOX treatment group changed obviously by using hematoxylin and eosin (H&E) staining assay, meanwhile cleaved caspase-3 (caspase-3) and tumor necrosis factor (TNF-alpha) were expressed at high levels tumors tissue in hydrogel/DOX treatment group by using immunohistochemical (IHC) staining. Doxorubicin 129-132 caspase 3 Homo sapiens 238-247 32770328-5 2021 Correspondingly, the analysis of histopathological morphology showed that the morphology and density of tumor tissue in hydrogel/DOX treatment group changed obviously by using hematoxylin and eosin (H&E) staining assay, meanwhile cleaved caspase-3 (caspase-3) and tumor necrosis factor (TNF-alpha) were expressed at high levels tumors tissue in hydrogel/DOX treatment group by using immunohistochemical (IHC) staining. Doxorubicin 129-132 caspase 3 Homo sapiens 249-258 33923922-7 2021 DOX markedly increased the generation of reactive oxygen species, PARP, caspase-3, and TUNEL-positive cell numbers, but reduced the expression of Bcl-2 and antioxidants" intracellular concentrations. Doxorubicin 0-3 caspase 3 Homo sapiens 72-81 33571711-4 2021 METHODS: We monitored DXR"s effect on aISCs by enumerating Lgr5-eGFP+ and Olfm4+ crypts, cleaved caspase-3 (CASP3+) immunofluorescence, and time-lapse organoid imaging. Doxorubicin 22-25 caspase 3 Homo sapiens 97-106 33571711-4 2021 METHODS: We monitored DXR"s effect on aISCs by enumerating Lgr5-eGFP+ and Olfm4+ crypts, cleaved caspase-3 (CASP3+) immunofluorescence, and time-lapse organoid imaging. Doxorubicin 22-25 caspase 3 Homo sapiens 108-113 32919690-7 2020 Furthermore, results of real-time quantitative PCR (RT-qPCR) and western blot analysis further validated the anticancer effect of FA-Ce6/DOX/BNPs, as evidenced by elevated gene/protein expression levels of apoptotic biomarkers p53, BID, caspase-3, cleaved poly(ADP-ribose) polymerase 1 (PARP-1), and BAX, contrary to levels of the anti-apoptotic marker Bcl-2. Doxorubicin 137-140 caspase 3 Homo sapiens 237-246 33390801-13 2021 Western blotting assay illustrated that the combination of USP37 knockdown with adriamycin treatment significantly upregulated the expression levels of cleaved caspase 3 and Bax, whereas the expression level of Bcl-2 was inhibited. Doxorubicin 80-90 caspase 3 Homo sapiens 160-169 33298102-14 2020 A decreased number of apoptotic nuclei and a preserved myocardial ultrastructure were found in all groups receiving prophylactic cardioprotection, while the DOX-induced fibrotic remodelling and the increase in caspase-3 levels could only be substantially prevented by the BB and ACEI treatments. Doxorubicin 157-160 caspase 3 Homo sapiens 210-219 32712543-12 2020 The FUC and DOX combination increased the levels and activity of caspases (CASP3, CASP8) and p53, while decreased the levels and activity of CYP3A4, GST, and PXR in resistant cancer cells. Doxorubicin 12-15 caspase 3 Homo sapiens 75-80 32851890-6 2020 Caspase-3/7 fluorescence assay was performed to detect apoptosis induction in PC-3 cells after treatment with the combinations of doxorubicin and OGT inhibitor to further understand the mechanism of cell death by concomitant treatment. Doxorubicin 130-141 caspase 3 Homo sapiens 0-11 32422307-7 2020 Moreover, the ability of DOX, TQ and TQ/DOX combination to induce apoptosis were analyzed by measuring caspase-3 expression using ELISA method. Doxorubicin 25-28 caspase 3 Homo sapiens 103-112 32422307-7 2020 Moreover, the ability of DOX, TQ and TQ/DOX combination to induce apoptosis were analyzed by measuring caspase-3 expression using ELISA method. Doxorubicin 40-43 caspase 3 Homo sapiens 103-112 32422307-11 2020 Also, TQ/DOX combination improved apoptosis by increasing caspase-3 expression and decreasing of BCL-2 expression. Doxorubicin 9-12 caspase 3 Homo sapiens 58-67 31630586-8 2020 Significant increased activation of TNF-alpha, Caspase-3 activity and myocardial infarct size in DOX-treated group. Doxorubicin 97-100 caspase 3 Homo sapiens 47-56 32647151-7 2020 Gene expression studies revealed a significant downregulation of TOP II and Ku70, crucial enzymes for DNA repair and replication, as well as MiR-155 oncogene, concomitant with an upregulation of caspase 3 and tumor suppressors i.e., p53, MEG3 and GAS5, in U251 cells upon treatment with DOX-EDT-IONPs. Doxorubicin 287-290 caspase 3 Homo sapiens 195-204 32620145-7 2020 SiRNA-mediated knockdown of LINC00426 remarkably compromised cell viability and proliferation in Dox-resistant OS cells, which accompanied with decrease of IC50 and activation of caspase-3. Doxorubicin 97-100 caspase 3 Homo sapiens 179-188