PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 35245520-3 2022 KEY FINDINGS: TQ monotherapy had greater anticancer effects to active VD3 or 5-FU, revealing higher expression of p21/p27/PTEN/BAX/Cyto-C/Casp-3 and increased levels of total glutathione, with inhibitions in CCND1/CCND3/BCL-2 and PI3K/AKT/mTOR molecules, alongside higher rates of apoptosis in HT29, SW480 and SW620 cells (P < 0.005 for all markers). Fluorouracil 77-81 caspase 3 Homo sapiens 138-144 34627212-9 2021 The activity of caspase 3 was increased by 5-FU but reduced by all concentrations of various extracts of BC. Fluorouracil 43-47 caspase 3 Homo sapiens 16-25 34185243-7 2021 RESULTS: The current study showed that 5FU succeeded in inducing cardiotoxicity, manifested by significantly elevated levels of cardiac enzymes, tissue malondialdehyde (MDA), interleukin 6 (IL-6), signal transducer and activator of transcription 4 (STAT4), and caspase-3. Fluorouracil 39-42 caspase 3 Homo sapiens 261-270 35596172-10 2022 We showed that the apoptotic markers, cleaved PARP and cleaved caspase-3, increased combining miR-675-5p inhibition with 5-FU treatment. Fluorouracil 121-125 caspase 3 Homo sapiens 63-72 32945504-7 2020 We also found that combined treatment of Rg3 and 5-FU significantly enhanced the apoptosis of colon cancer cells by activating the Apaf1/caspase 9/caspase 3 pathway and arrested the cell cycle of the colon cancer cells in G0/G1 by promoting the expression of Cyclin D1, CDK2 and CDK4. Fluorouracil 49-53 caspase 3 Homo sapiens 147-156 35326689-11 2022 Moreover, 5-FU/VD3/Met revealed maximal inhibitions of cell cycle inducers (CCND1/CCND3), cell survival (BCL2), and the PI3K/Akt/mTOR molecules alongside the highest expression of cell cycle inhibitors (p21/p27), proapoptotic markers (BAX/cytochrome C/caspase-3), and PTEN in both cell lines. Fluorouracil 10-14 caspase 3 Homo sapiens 252-261 35416117-6 2022 When 5-FU (5 microM) was administered, the percentage of apoptotic cells, cytochrome C release and caspase-3 activity was found to be higher in the shDDR1a group than that in the control group. Fluorouracil 5-9 caspase 3 Homo sapiens 99-108 35191521-6 2022 In vitro, the AZD6738/5-FU combination increased the number of mitotic cells according to flow cytometry, decreased the checkpoint kinase 1 phosphorylation levels and increased cleaved caspase-3 and phosphorylated form of H2A.X variant histone levels according to western blotting, and decreased the proliferation rate of four colon cancer cell lines according to cell viability experiments. Fluorouracil 22-26 caspase 3 Homo sapiens 185-194 30990333-3 2021 The combination of PGG and 5-FU had synergistic effects on reversal the aggressive phenotypes of HepG2 cells, increasing the proportion of Bax/Bcl-2, promoting the activation of caspase-9 and caspase-3, and inducing apoptosis. Fluorouracil 27-31 caspase 3 Homo sapiens 192-201 32665777-10 2020 Moreover, qPCR analyses showed that CASP3 and CASP9 mRNA levels significantly increased after pre-treatment with Pxd followed by 5-Fu and 1-OHP treatments, compared to 5-Fu with 1-OHP alone. Fluorouracil 129-133 caspase 3 Homo sapiens 36-41 32975155-3 2020 Results: Combination treatment with 5-FU and radiation had a stronger effect on decreasing Bcl-2 expression and increasing expression of Bax, cleaved caspase-9, cleaved caspase-3, cleaved PARP compared with each treatment alone. Fluorouracil 36-40 caspase 3 Homo sapiens 169-178 32665777-10 2020 Moreover, qPCR analyses showed that CASP3 and CASP9 mRNA levels significantly increased after pre-treatment with Pxd followed by 5-Fu and 1-OHP treatments, compared to 5-Fu with 1-OHP alone. Fluorouracil 168-172 caspase 3 Homo sapiens 36-41 32509181-12 2020 In addition, the combination treatment (emodin plus 5-Fu) induced cell apoptosis via inhibiting Bcl-2 and activating cleaved caspase3 and Bax. Fluorouracil 52-56 caspase 3 Homo sapiens 125-133 31352611-4 2019 Our results revealed 5-FU preferably induces marked apoptosis in BRAF-mutant colorectal cancer cells, through attenuating expression of Bcl-xL and activation caspase-3/9 pathway, eventually conferring the anti-tumor efficacy of 5-FU in vitro and in vivo. Fluorouracil 21-25 caspase 3 Homo sapiens 158-169 31969973-9 2020 We further demonstrated that FAK silencing increased 5-FU-induced caspase-3 activity, and promoted p53 transcriptional activities. Fluorouracil 53-57 caspase 3 Homo sapiens 66-75 33489855-7 2021 Unlike AGS FR cells, AGS cells showed increased levels of both cleaved caspase-3 and Bax following 5-FU treatment. Fluorouracil 99-103 caspase 3 Homo sapiens 71-80 31753399-6 2020 The expression of Caspase-3 and Caspase-9 apoptosis-related protein levels was slightly upregulated and Atg5 autophagy-related protein level was clearly downregulated according to control and 5-FU-treated cells after complex I and II treatment. Fluorouracil 192-196 caspase 3 Homo sapiens 18-27 31352611-4 2019 Our results revealed 5-FU preferably induces marked apoptosis in BRAF-mutant colorectal cancer cells, through attenuating expression of Bcl-xL and activation caspase-3/9 pathway, eventually conferring the anti-tumor efficacy of 5-FU in vitro and in vivo. Fluorouracil 228-232 caspase 3 Homo sapiens 158-169 30915129-4 2019 Functionally, miR-214 inhibited cell clone formation and cell growth and enhanced 5-FU-inducing cell apoptosis and caspase-3 levels. Fluorouracil 82-86 caspase 3 Homo sapiens 115-124 31623083-4 2019 RESULTS: The results of this study indicate that 5-FU differentially affects superoxide production and caspase-3 activation when applied in cytotoxic concentrations against HeLa cells, while superoxide accumulation is in accordance with mitochondrial superoxide levels. Fluorouracil 49-53 caspase 3 Homo sapiens 103-112 31072625-12 2019 Additionally, transfection of miR-145 mimic further altered expression of key genes involved in cell apoptosis (Bcl-2, Bax, Caspase3) in ESCC cells treated with 5-FU. Fluorouracil 161-165 caspase 3 Homo sapiens 124-132 29695684-9 2018 Moreover, 5-fluorouracil plus circularly permuted tumor necrosis factor-related apoptosis-inducing ligand increased apoptosis-related protein levels such as cleaved caspase-3, caspase-8, and poly-ADP-ribose polymerase and downregulated that of the survival protein B-cell lymphoma-extra-large. Fluorouracil 10-24 caspase 3 Homo sapiens 165-174 30328537-11 2018 Western blot analysis clearly showed that 5-FU and LY individually increased the expression of caspase-3 and PARP, while as expected FLNP induced a remarkable expression of these protein markers indicating the superior anticancer effect. Fluorouracil 42-46 caspase 3 Homo sapiens 95-104 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. Fluorouracil 87-91 caspase 3 Homo sapiens 172-181 30741544-9 2019 The accumulation of 5-FU resulted in caspase-3 and PARP activation, Bcl-2 reduction, and Bad increase, which ultimately lead to cancer cell apoptosis. Fluorouracil 20-24 caspase 3 Homo sapiens 37-46 31372308-13 2019 Gene expression of casp-3, casp-4, and casp-10 were significantly inhibited in the DCLK1+ cells after 5-Fu treatment compared to the WT cells (p=7.616e-08, 1.575e-05 and 5.307e-08, respectively). Fluorouracil 102-106 caspase 3 Homo sapiens 19-25 31372308-14 2019 Cleaved casp-3 amount and casp-3 positive cells were significantly decreased in the DCLK1+ cells after 5-Fu treatment compared to the WT cells (p=0.015). Fluorouracil 103-107 caspase 3 Homo sapiens 8-14 31372308-14 2019 Cleaved casp-3 amount and casp-3 positive cells were significantly decreased in the DCLK1+ cells after 5-Fu treatment compared to the WT cells (p=0.015). Fluorouracil 103-107 caspase 3 Homo sapiens 26-32 31949673-0 2018 Knockdown of PHGDH potentiates 5-FU cytotoxicity in gastric cancer cells via the Bcl-2/Bax/caspase-3 signaling pathway. Fluorouracil 31-35 caspase 3 Homo sapiens 91-100 31949673-12 2018 Additionally, 5-FU treatment downregulated Bcl-2 expression and upregulated the expression of Bax and caspase-3, and this effect was remarkably enhanced by PHGDH knockdown. Fluorouracil 14-18 caspase 3 Homo sapiens 102-111 31949673-13 2018 In conclusion, knockdown of PHGDH potentiates 5-FU cytotoxicity in GC cells via the Bcl-2/Bax/caspase-3 signaling pathway. Fluorouracil 46-50 caspase 3 Homo sapiens 94-103 29795190-4 2018 Enforced miR-181a expression enhanced 5-FU-induced p53-dependent mitochondrial apoptosis, including declined Bcl-2/Bax ratio, loss of mitochondrial membrane potential, cytochrome c release, and caspase-9 and caspase-3 activation. Fluorouracil 38-42 caspase 3 Homo sapiens 208-217 29601890-9 2018 Only 5-Fu or the knockdown of RPA1 suppressed cell clone formation, induced cell cycle arrest at the G1 phase and promoted cell apoptosis by regulating the protein level of Caspase 3. Fluorouracil 5-9 caspase 3 Homo sapiens 173-182 29921390-9 2018 The percentage of cell apoptosis increased, and the Western blot showed that the expression of caspase-3, caspase-8, and c-myc, respectively, in the semi-combination group, the 5-Fluorouracil group, and the combination group increased successively and that the successive increasing of c-myc was the most significant. Fluorouracil 177-191 caspase 3 Homo sapiens 95-104 26735343-8 2016 The RT-PCR assessment of caspase-3 expression revealed that there was a significant increase in caspase-3 expression in Hep-2 cell line treated with 5-fluorouracil nanoparticles or curcumin compared to non treated cancer cells. Fluorouracil 149-163 caspase 3 Homo sapiens 25-34 29719602-6 2018 In addition, leptin reduced the 5-FU effects on apoptosis by decreasing pro-apoptotic (Bax, Caspase-3 activation and PARP degradation) and increasing anti-apoptotic factors (RIP and Bcl-XL). Fluorouracil 32-36 caspase 3 Homo sapiens 92-101 29277783-6 2018 In addition, both chemical and genetic inhibition of HDAC1 reduced the activation of caspase-3 and cytotoxicity in 5-fluorouracil (5FU)-treated cancer cells. Fluorouracil 115-129 caspase 3 Homo sapiens 85-94 29277783-6 2018 In addition, both chemical and genetic inhibition of HDAC1 reduced the activation of caspase-3 and cytotoxicity in 5-fluorouracil (5FU)-treated cancer cells. Fluorouracil 131-134 caspase 3 Homo sapiens 85-94 29183726-8 2018 Moreover, there were large bubbles blowing from the membrane of 5-FU-treated cells and the cleavage of GSDME but not GSDMD, which were blocked by the silence or specific inhibitor of caspase-3. Fluorouracil 64-68 caspase 3 Homo sapiens 183-192 29209153-7 2017 5-Fluorouracil and oxaliplatin treatment lead to an enhanced caspase 3-dependent apoptosis and produce an increase of autophagy. Fluorouracil 0-14 caspase 3 Homo sapiens 61-70 28870916-5 2017 In the presence of 5-FU, GRP78 knockdown induced apoptosis via activation of caspase-3 and poly(ADP-ribose)-polymerase 1. Fluorouracil 19-23 caspase 3 Homo sapiens 77-86 28440463-11 2017 Consistent with this, Livin-knockdown cells showed greater expression of cleaved caspases-3 and -7 and poly(ADP-ribose)polymerase compared with that in control cells after cisplatin, 5-FU, or docetaxel treatment. Fluorouracil 183-187 caspase 3 Homo sapiens 81-98 28454373-8 2017 In SGC7901 cells, protein expression of active caspase-3 and cleaved poly (ADP-ribose) polymerase was increased following treatment with 5-FU, while phosphorylated Akt serine/threonine kinase 1 (Akt) levels were decreased. Fluorouracil 137-141 caspase 3 Homo sapiens 47-56 27509880-0 2016 Combination of the histone deacetylase inhibitor depsipeptide and 5-fluorouracil upregulates major histocompatibility complex class II and p21 genes and activates caspase-3/7 in human colon cancer HCT-116 cells. Fluorouracil 66-80 caspase 3 Homo sapiens 163-174 27509880-3 2016 Exposure to a combination of 5-FU (1.75 microM) and 1 nM depsipeptide for 24 and 48 h resulted in a 3- to 4-fold increase in activated caspase-3/7, while 5-FU alone failed to activate caspase-3/7. Fluorouracil 29-33 caspase 3 Homo sapiens 135-144 27509880-3 2016 Exposure to a combination of 5-FU (1.75 microM) and 1 nM depsipeptide for 24 and 48 h resulted in a 3- to 4-fold increase in activated caspase-3/7, while 5-FU alone failed to activate caspase-3/7. Fluorouracil 29-33 caspase 3 Homo sapiens 135-146 27509880-4 2016 Microarray and subsequent gene ontology analyses revealed that compared to 5-FU or depsipeptide alone, the combination treatment of 5-FU and depsipeptide upregulated genes related to cell death and the apoptotic process consistent with the inhibition of colony formation and caspase-3/7 activation. Fluorouracil 132-136 caspase 3 Homo sapiens 275-284 27144434-6 2016 Using genetic and pharmacological approaches, we showed that ERK5 inhibition increased caspase-3/7 activity and apoptosis following 5-FU exposure. Fluorouracil 132-136 caspase 3 Homo sapiens 87-96 26845645-4 2016 Importantly, overexpression of miR-450b-5p in 5-FU-resistant HT-29 cells reduced cell viability, but elevated DNA fragmentation levels and caspase-3 activity were induced by treatment with 5-FU. Fluorouracil 46-50 caspase 3 Homo sapiens 139-148 26845645-4 2016 Importantly, overexpression of miR-450b-5p in 5-FU-resistant HT-29 cells reduced cell viability, but elevated DNA fragmentation levels and caspase-3 activity were induced by treatment with 5-FU. Fluorouracil 189-193 caspase 3 Homo sapiens 139-148 26662569-8 2016 The expression of PCNA and Bcl-XL is remarkably decreased, and the expression of Caspase-3 and cleaved Caspase-3 is obviously increased in GC cells treated with the single and combination of 5-Fu and PD. Fluorouracil 191-195 caspase 3 Homo sapiens 81-112 28599477-9 2017 The combination of SM-1 and 5-FU treatment led to significantly increased caspase-3 activity compared with either compound alone. Fluorouracil 28-32 caspase 3 Homo sapiens 74-83 28349835-6 2017 Deglycosylation of epithelial cell adhesion molecule enhanced the cytotoxic effect of 5-fluorouracil, promoting apoptosis by downregulating the expression of the anti-apoptotic protein Bcl-2 and upregulating the expression of the pro-apoptotic proteins Bax and Caspase 3 via the extracellular-signal-regulated kinase 1/2 and c-Jun N-terminal kinase mitogen-activated protein kinase signaling pathways in MCF-7 and MDA-MB-231 cells. Fluorouracil 86-100 caspase 3 Homo sapiens 261-270 28296564-5 2017 Combination therapy also increased the amount of caspase-3 dependent apoptosis compared with 5-FU alone (4% vs. 13%). Fluorouracil 93-97 caspase 3 Homo sapiens 49-58 26392056-7 2016 The observed synergistic interaction of both PBOX-15/Oxaliplatin and PBOX-15/5FU may involve activation of p38 MAPK and JNK pathway, which in turn significantly increased caspase-3 cleavage in DLD-1 cells, treated with PBOX-5/Oxaliplatin but not with PBOX-15/5FU. Fluorouracil 77-80 caspase 3 Homo sapiens 171-180 26735343-8 2016 The RT-PCR assessment of caspase-3 expression revealed that there was a significant increase in caspase-3 expression in Hep-2 cell line treated with 5-fluorouracil nanoparticles or curcumin compared to non treated cancer cells. Fluorouracil 149-163 caspase 3 Homo sapiens 96-105 26432329-8 2016 The single and combination of 5-Fu and BGJ398 decreased the expressions of PCNA, Bcl-xl, and FLIP while increased the expression of caspase-3 in GC cells, especially in shRNA groups. Fluorouracil 30-34 caspase 3 Homo sapiens 132-141 26844701-0 2016 Low levels of Caspase-3 predict favourable response to 5FU-based chemotherapy in advanced colorectal cancer: Caspase-3 inhibition as a therapeutic approach. Fluorouracil 55-58 caspase 3 Homo sapiens 14-23 26844701-10 2016 Exposure of explant cultures to 5FU-based CT increased the percentage of cells positive for active Caspase-3 and Terminal Deoxynucleotidyl Transferase dUTP Nick end Labelling (TUNEL), but also the expression of regeneration and proliferation markers beta-Catenin and Ki-67, as well as cyclooxygenase-2 (COX-2). Fluorouracil 32-35 caspase 3 Homo sapiens 99-108 26691280-12 2016 Results indicated that 5-FU decreased H-ras, Rho-A, p53, Stat1 and increased Bax gene expression in Tumor2 and decreased Rac1, Rho-A, NF-kappaB and increased Bax and caspase-3 protein expression in Tumor2. Fluorouracil 23-27 caspase 3 Homo sapiens 166-175 26691280-14 2016 5-FU decreased Rac1, Rho-A protein expression and increased Bax and caspase-3 protein expression in MDA-MB-231. Fluorouracil 0-4 caspase 3 Homo sapiens 68-77 26462739-6 2016 Consistently, costimulation of HeLa cells with any chemotherapeutic agent in the presence of melatonin further increased caspase-3 activation, particularly in CIS- and 5-FU-challenged cells. Fluorouracil 168-172 caspase 3 Homo sapiens 121-130 26893778-7 2016 Therefore, the downregulation of Foxc2, induced by 5-FU, may enhance apoptosis by the downregulation of apoptotic factors, including B cell lymphoma-2 and pro-caspase-3, in Foxc2-shRNA CRC cells. Fluorouracil 51-55 caspase 3 Homo sapiens 140-168 26810644-6 2016 To assess the short-term cytotoxicity and examine the apoptotic effects upon addition of 5-FU in vitro, we performed LIVE/DEAD and caspase-3 activity assays. Fluorouracil 89-93 caspase 3 Homo sapiens 131-140 26810644-10 2016 While both 5-FU and/or trastuzumab-IR700 conjugate treatment induced an increase in caspase-3 activity, there was no additional increase in caspase-3 activity upon NIR light irradiation after incubation with 5-FU and/or trastuzumab-IR700. Fluorouracil 11-15 caspase 3 Homo sapiens 84-93 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. Fluorouracil 15-19 caspase 3 Homo sapiens 114-123 26692822-13 2015 In addition, As2O3 in combination with 5-FU treatment caused up-regulation of DR5, caspase 3, caspase 8, and caspase 9, and down-regulation of BCL-2, but had no effect of DR4. Fluorouracil 39-43 caspase 3 Homo sapiens 83-92 25348361-9 2015 In conclusion, DNA-PKcs suppression had complementary effects in combination with CDDP and 5-Fu treatment in HepG2 cells, which was associated with suppression of NF-kappaB signaling pathway cascade, activation of caspase-3 and p53, as well as down-regulation of Bcl-2 and GSH. Fluorouracil 91-95 caspase 3 Homo sapiens 214-223 26788191-9 2015 Furthermore, 5-FU upregulated caspase-3 and caspase-9, promoting apoptosis in TUSC4-overexpressing cells compared with cells that were transduced with TUSC4 or treated with 5-FU and NC cells. Fluorouracil 13-17 caspase 3 Homo sapiens 30-39 25906152-2 2015 We generated caspase-3 knockout (C3KO) and knockdown human colorectal cancer cells, and found that they are unexpectedly sensitized to DNA-damaging agents including 5-fluorouracil (5-FU), etoposide, and camptothecin. Fluorouracil 165-179 caspase 3 Homo sapiens 13-22 25906152-2 2015 We generated caspase-3 knockout (C3KO) and knockdown human colorectal cancer cells, and found that they are unexpectedly sensitized to DNA-damaging agents including 5-fluorouracil (5-FU), etoposide, and camptothecin. Fluorouracil 181-185 caspase 3 Homo sapiens 13-22 25906152-6 2015 5-FU treatment led to the formation of a z-VAD-resistant pro-caspase-8/RIP1/FADD complex, which was strongly stabilized by caspase-3 KO. Fluorouracil 0-4 caspase 3 Homo sapiens 123-132 25736303-8 2015 The combination of 5-FU and Res significantly increased the percentage of apoptotic cells and the level of activated caspase-3, cleaved PARP and p53 proteins as well as increased the Bax/Bcl-2 ratio. Fluorouracil 19-23 caspase 3 Homo sapiens 117-126 25643258-3 2015 Compared with the sole use of each agent, PHA-767491 in combination with 5-FU exhibited much stronger cytotoxicity and induced significant apoptosis manifested by remarkably increased caspase 3 activation and poly(ADP-Ribose) polymerase fragmentation in HCC cells. Fluorouracil 73-77 caspase 3 Homo sapiens 184-193 25333998-7 2015 Further, 5-FU attenuated SNX-2112-induced apoptosis by decreasing poly(ADP-ribose) polymerase (PARP) cleavage and inactivating caspase-3, -8 and -9. Fluorouracil 9-13 caspase 3 Homo sapiens 127-147 25149123-9 2014 Moreover, 5-fluorouracil (5-Fu) loaded FA-CM-beta-CD-BSA NPs down-regulate ATP levels and increase the expression of caspase-3. Fluorouracil 10-24 caspase 3 Homo sapiens 117-126 25149123-9 2014 Moreover, 5-fluorouracil (5-Fu) loaded FA-CM-beta-CD-BSA NPs down-regulate ATP levels and increase the expression of caspase-3. Fluorouracil 26-30 caspase 3 Homo sapiens 117-126 25788859-11 2014 Decreased Survivin, Cyclin D, Bcl-2, and increased Caspase-3, P53 expression level were aslo confirmed by western blot in 5-fluorouracil combine with myricetin groups in vitro. Fluorouracil 122-136 caspase 3 Homo sapiens 51-60 23946796-8 2013 Knockdown of HuR apparently abrogated 5-FU-induced apoptosis detected by caspase-3 activities. Fluorouracil 38-42 caspase 3 Homo sapiens 73-82 24249161-6 2014 The activity of caspases-3, -7, and -9 were also assessed in miR-23a antisense and 5-FU treated tumor cells. Fluorouracil 83-87 caspase 3 Homo sapiens 16-38 25087947-8 2014 Furthermore, combination treatment of GNA and 5-FU showed up-regulated of caspase-3, caspase-9, bax, RIP1, apoptosis-inducing factor (AIF), voltage-dependent anion channel (VDAC), cytochrome c and cyclophilin D and down-regulated bcl-2. Fluorouracil 46-50 caspase 3 Homo sapiens 74-83 24190362-9 2014 In addition, hTERTC27 overexpression evidently promoted the 5-FU-induced apoptosis by increasing the expression of activated caspase-3 and -9 and by downregulating the expression of B-cell lymphoma 2. Fluorouracil 60-64 caspase 3 Homo sapiens 125-141 23619566-7 2013 Further investigation revealed that NK4 gene expression enhanced 5-FU-induced caspase-3 and caspase-9 activation, and that the apoptosis of cells was associated with modulation of expression of the Bcl-2 family members. Fluorouracil 65-69 caspase 3 Homo sapiens 78-87 23349734-11 2013 The cleaved caspase-3 expression was significantly decreased (2.09 and 2.47 folds respectively for 5-Fluorouracil and Camptothecin) in H460 spheroid cultures compared to 2D culture system. Fluorouracil 99-113 caspase 3 Homo sapiens 12-21 22773580-9 2012 None of the compounds induced internucleosomal DNA fragmentation and only 5-FU induced slight activation of caspase-3 in an oral squamous cell carcinoma cell line (HSC-2). Fluorouracil 74-78 caspase 3 Homo sapiens 108-117 22607196-6 2012 The synergistic effect of 5-FU induced by oroxylin A was also found in the suppression of Bcl-2 and in the activation of P53, Bax, PARP, and procaspase-3 proteins in HT-29 cells. Fluorouracil 26-30 caspase 3 Homo sapiens 141-153 22206670-5 2012 Moreover, we found that TQ enhanced the 5-FU-induced killing of gastric cancer cells by mediating the downregulation of the anti-apoptotic protein bcl-2, the upregulation of the pro-apoptotic protein bax, and the activation of both caspase-3 and caspase-9. Fluorouracil 40-44 caspase 3 Homo sapiens 232-241 22244588-0 2012 Synthesis and biological evaluation of conjugates of deoxypodophyllotoxin and 5-FU as inducer of caspase-3 and -7. Fluorouracil 78-82 caspase 3 Homo sapiens 97-113 22265744-6 2012 Furthermore, CDy::UPRT-MSCs were significantly more sensitive to 5-fluorouracil (5FU), cisplatin, cyclophosphamide and cytosine arabinoside as determined by increased Caspase 3/7 activation and/or decreased relative proliferation. Fluorouracil 65-79 caspase 3 Homo sapiens 167-176 22265744-6 2012 Furthermore, CDy::UPRT-MSCs were significantly more sensitive to 5-fluorouracil (5FU), cisplatin, cyclophosphamide and cytosine arabinoside as determined by increased Caspase 3/7 activation and/or decreased relative proliferation. Fluorouracil 81-84 caspase 3 Homo sapiens 167-176 22206670-7 2012 These data suggest that the TQ/5-FU combined treatment induces apoptosis by enhancing the activation of both caspase-3 and caspase-9 in gastric cancer cells. Fluorouracil 31-35 caspase 3 Homo sapiens 109-118 22206670-8 2012 These results, which provide molecular evidence both in vitro and in vivo, support our conclusion that thymoquinone can activate caspase-3 and caspase-9 and thus result in the chemosensitisation of gastric cancer cells to 5-FU-induced cell death. Fluorouracil 222-226 caspase 3 Homo sapiens 129-138 21403907-9 2011 Moreover, compared with 5-FU alone, the apoptosis of CRC cells treated with DCA and 5-FU was enhanced and demonstrated with the changes of Bcl-2, Bax, and caspase-3 proteins. Fluorouracil 84-88 caspase 3 Homo sapiens 155-164 22002472-6 2012 The protein expression of Bax and caspase-3 in the J5 xenograft tumors treated with Tan-IIA 30 mg/-kg or with 30 mg/kg of 5-FU was upregulated, whereas that of CD31 was downregulated compared with the control group. Fluorouracil 122-126 caspase 3 Homo sapiens 34-43 21375586-9 2011 Caspase-3 activation was significantly lower in the co-treated group than in the group treated with 5-FU alone. Fluorouracil 100-104 caspase 3 Homo sapiens 0-9 20876774-9 2011 Mechanistic studies revealed that 5-FU-mediated suppression of c-FLIP results in increased TRAIL-induced recruitment and activation of caspase-8 at the death-inducing signalling complex (DISC), leading to caspase-3 activation and caspase-dependent cell death. Fluorouracil 34-38 caspase 3 Homo sapiens 205-214 19793002-6 2009 The downregulation of cIAP2 efficiently enhances apoptosis through the activation of caspase 3/7 and 5-fluorouracil (5-FU) sensitivity in colorectal cancer cells exposed to 5-FU. Fluorouracil 173-177 caspase 3 Homo sapiens 85-94 21461573-0 2011 Chan-Yu-Bao-Yuan-Tang and 5-fluorouracil synergistically induce apoptosis by means of the caspase-3 signaling pathway in lung and cervical cancer cells. Fluorouracil 26-40 caspase 3 Homo sapiens 90-99 21461573-7 2011 CYBYT and 5-Fu, alone or in combination, up-regulated cleaved caspase-3 expression in a time-dependent manner, with CYBYT being more effective than 5-Fu. Fluorouracil 10-14 caspase 3 Homo sapiens 62-71 22216150-8 2011 Induction of Bcl-2 expression by HBV pre-S2Delta protein resulted in resistance to 5-fluorouracil treatment in colony formation, caspase-3 assay, and cell apoptosis, and can enhance cell death by co-incubation with Bcl-2 inhibitor. Fluorouracil 83-97 caspase 3 Homo sapiens 129-138 19585117-10 2010 Western blotting assay revealed oroxylin A enhanced 5-FU-induced apoptosis in HepG2 cells by elevating the expressions of apoptotic-inducing proteins P53 and cleaved PARP and decreasing the expression of apoptotic-inhibitory proteins COX-2, Bcl-2, and pro-caspase3. Fluorouracil 52-56 caspase 3 Homo sapiens 252-264 19903580-5 2010 PG490 and 5-FU treatment induced activated caspase 3 and Bax expression and inhibited Bcl-2 expression. Fluorouracil 10-14 caspase 3 Homo sapiens 43-52 19302291-6 2009 The down-regulation of cIAP2 efficiently enhanced 5-FU sensitivity, the activation of caspase 3/7 and apoptosis under exposure to 5-FU. Fluorouracil 130-134 caspase 3 Homo sapiens 86-95 18082672-8 2008 In addition, the combination 5-FU plus scFv23/TNF induced apoptosis and this synergistic effect was dependent on activation of caspase-8 and caspase-3. Fluorouracil 29-33 caspase 3 Homo sapiens 141-150 19097688-8 2009 Surprisingly, the addition of ANDRO to 5-FU induces synergistic apoptosis, which could be corroborated to the increased caspase-8, p53 activity and the significant changes of Bax conformation in these cells, resulting in increased losses of mitochondrial membrane potential, increased release of cytochrome c, and activation of caspase-9 and caspase-3. Fluorouracil 39-43 caspase 3 Homo sapiens 342-351 18606591-5 2008 CDDP and 5-FU induced apoptosis mediated by the intrinsic pathway in colon cancer cells, as demonstrated by morphological analyses, mitochondrial cytochrome c release and cleavage of caspase 3. Fluorouracil 9-13 caspase 3 Homo sapiens 183-192 17363540-11 2007 Moreover, this technique sheds light on the synergy of 5-FU and TRAIL as evidenced by differences in the temporal activation of caspase-3 resulting from the different therapeutic regimens. Fluorouracil 55-59 caspase 3 Homo sapiens 128-137 17805550-2 2008 This study evaluates the putative clinical usefulness of measuring caspase-3 activity as a prognostic factor in colonic cancer patients receiving 5-fluoracil adjuvant chemotherapy. Fluorouracil 146-157 caspase 3 Homo sapiens 67-76 17805550-11 2008 CONCLUSION: Low caspase-3 activity in the normal mucosa and tumour are independent prognostic factors of tumour recurrence in patients receiving adjuvant 5-fluoracil-based treatment in colon cancer, correlating with poor disease-free survival and higher recurrence rate. Fluorouracil 154-165 caspase 3 Homo sapiens 16-25 17399942-13 2007 Using an antibody that recognizes unprocessed caspase-3, we observed that the enzyme was assumingly activated in HepG2 cells treated with 5FU and paclitaxel, but only weakly after treatment with cisplatin. Fluorouracil 138-141 caspase 3 Homo sapiens 46-55 17439729-9 2007 Insulin/5-FU treatment enhanced apoptosis of tumor cells and upregulated the expression of cleaved caspase-3 compared with 5-FU treatment. Fluorouracil 8-12 caspase 3 Homo sapiens 99-108 17045692-7 2007 Caspase-3 activation was exclusively increased by IFNalpha/5-FU combination treatment, which was compatible with enhancement of the synergistic apoptotic effect, and other caspases and apoptotic factors (FLIP, BCL-xl, and Bax) were also regulated by IFNalpha/5-FU. Fluorouracil 259-263 caspase 3 Homo sapiens 0-9 17056233-9 2007 Nuclear fragmentation and caspase-3, -8 and -9 activities were also markedly increased in HCT116 cells after 5-FU (p<0.001). Fluorouracil 109-113 caspase 3 Homo sapiens 26-46 15608676-14 2005 Additionally, we show that Chk1 deficiency potentiates 5-FU efficacy through the preferential induction of the caspase-8 pathway and subsequent caspase-3 activation. Fluorouracil 55-59 caspase 3 Homo sapiens 144-153 17045692-7 2007 Caspase-3 activation was exclusively increased by IFNalpha/5-FU combination treatment, which was compatible with enhancement of the synergistic apoptotic effect, and other caspases and apoptotic factors (FLIP, BCL-xl, and Bax) were also regulated by IFNalpha/5-FU. Fluorouracil 59-63 caspase 3 Homo sapiens 0-9 17016659-7 2006 Caspase-3, -9, and especially caspase-8 activity was higher with IFN alpha plus 5-FU than IFN or 5-FU alone. Fluorouracil 80-84 caspase 3 Homo sapiens 0-13 15546879-7 2005 Protein and transcriptome expression analysis showed that combined 5-FU and DENSPM treatment activated caspase 9, but not caspase 3, and significantly suppressed NADH dehydrogenases and cytochrome c oxidases, consistent with the observed increase in hydrogen peroxide, loss of mitochondrial membrane potential, and release of cytochrome c. Fluorouracil 67-71 caspase 3 Homo sapiens 122-131 16491956-8 2005 In these cells, both caspase-3 and -9 were involved in the activation of apoptosis after CPT-11/5-FU treatment. Fluorouracil 96-100 caspase 3 Homo sapiens 21-37 15684607-7 2005 However, the chemotherapeutic agent 5-FU, by inducing Caspase-1 and Caspase-3 activation, induced secretion of proteolytically processed mature and degraded IL-18 species, respectively, in Capan-2 cells. Fluorouracil 36-40 caspase 3 Homo sapiens 68-77 15282376-6 2004 Finally, 5-fluorouracil and docetaxel were shown to cause apoptotic cell death involving caspase-3 cleavage in Centre d"Etude du Polymorphisme Humain lymphoblastoid cells. Fluorouracil 9-23 caspase 3 Homo sapiens 89-98 15585135-7 2004 Our experiments showed that 5-FU engaged the mitochondrial apoptotic pathway involving cytosolic cytochrome c release and subsequent activation of caspase-9 and caspase-3 as well as the membrane death receptor (DR)-mediated apoptotic pathway involving activation of caspase-8 with an Apo-1/CD95 (Fas)-dependent fashion. Fluorouracil 28-32 caspase 3 Homo sapiens 161-170 12773255-0 2003 [Role of caspase-8 and caspase-3 in hepatoma cells apoptosis induced by 5-fluorouracil]. Fluorouracil 72-86 caspase 3 Homo sapiens 23-32 15124184-5 2004 In the present experiments, we examined the expression of caspase-3, p53 and Bid in the three cell lines induced by 5-FU and/or anti-CD8 antibody. Fluorouracil 116-120 caspase 3 Homo sapiens 58-67 15124184-7 2004 We also detected the active form of caspase-3 and Bid in apoptotic leukemia cells after treatment with 5-FU and/or anti-CD8 antibody, indicating that the drug and antibody induced cell death through caspase-3 and the signal pathway may involve the Bcl-2 protein family. Fluorouracil 103-107 caspase 3 Homo sapiens 36-45 15124184-7 2004 We also detected the active form of caspase-3 and Bid in apoptotic leukemia cells after treatment with 5-FU and/or anti-CD8 antibody, indicating that the drug and antibody induced cell death through caspase-3 and the signal pathway may involve the Bcl-2 protein family. Fluorouracil 103-107 caspase 3 Homo sapiens 199-208 15124184-8 2004 Our results showed that combined treatment with 5-FU and anti-CD8 antibody could enhance the rate of apoptosis induced by 5-FU or anti-CD8 antibody through increased expression of p53 and by promoting activation of caspase-3 and Bid. Fluorouracil 48-52 caspase 3 Homo sapiens 215-224 15124184-8 2004 Our results showed that combined treatment with 5-FU and anti-CD8 antibody could enhance the rate of apoptosis induced by 5-FU or anti-CD8 antibody through increased expression of p53 and by promoting activation of caspase-3 and Bid. Fluorouracil 122-126 caspase 3 Homo sapiens 215-224 15120327-5 2004 Whereas treatment with the combination of TRAIL and 5-FU or mitomycin led to enhanced activation of caspase-3, the combination of TRAIL and calpain inhibitor I resulted in enhanced activation of both caspase-8 and caspase-3. Fluorouracil 52-56 caspase 3 Homo sapiens 100-109 12915131-2 2003 Further studies revealed that the cells susceptible to 5-FU treatment died of apoptosis, which was demonstrated by caspase-3 activation, loss of mitochondria membrane potential (MMP), and DNA fragmentation. Fluorouracil 55-59 caspase 3 Homo sapiens 115-124 12941601-5 2003 5-FU also resulted in an increase in the number of TUNEL-positive cells and enhanced caspase-3 activity 3- to 5-fold in NUGC3 cells but not NUGC3/5FU/L cells. Fluorouracil 0-4 caspase 3 Homo sapiens 85-94 15015643-7 2003 Compared with normal group, 5-Fu and antisense survivin group, the cells growth inhibition, apoptosis index, and caspase-3 activity were increased in antisense survivin transfected + 5-Fu group. Fluorouracil 183-187 caspase 3 Homo sapiens 113-122 12934351-1 2003 OBJECTIVES: To study the change of caspase-3 activity on the neoadjuvant chemotherapy-induced apoptosis by hydroxycamptothecin (HCPT) with 5-fluorouracil (5-Fu)/leucovorin (CF) in large-intestinal carcinoma, and to explore its mechanism. Fluorouracil 139-153 caspase 3 Homo sapiens 35-44 12934351-1 2003 OBJECTIVES: To study the change of caspase-3 activity on the neoadjuvant chemotherapy-induced apoptosis by hydroxycamptothecin (HCPT) with 5-fluorouracil (5-Fu)/leucovorin (CF) in large-intestinal carcinoma, and to explore its mechanism. Fluorouracil 155-159 caspase 3 Homo sapiens 35-44 26680854-12 2002 Furthermore, 5-FU increased the enzymatic activity of caspase-3 protease with PARP digestion in HepG2 cells. Fluorouracil 13-17 caspase 3 Homo sapiens 54-63 12414664-7 2002 NSAIDs and 5-FU induced the mitochondrial release of cytochrome c as well as caspase-3 and -9 activation, and to a much lesser extent, caspase-8. Fluorouracil 11-15 caspase 3 Homo sapiens 77-93 11408917-0 2001 Activation of caspase-3 in renal cell carcinoma cells by anthracyclines or 5-fluorouracil. Fluorouracil 75-89 caspase 3 Homo sapiens 14-23 11836567-15 2002 Although the receptor signaling pathway in apoptosis was not observed by 5-FU, Bax-induced cytochrome c and caspase 3 was also observed in a receptor-independent pathway by 5-FU and CDDP. Fluorouracil 173-177 caspase 3 Homo sapiens 108-117 11408917-8 2001 Of the six freshly derived RCC cells treated with 5-FU, caspase-3 activity was increased 3.1-fold (p = 0.0051) and 2.4-fold (p = 0.0346) in two of them, respectively. Fluorouracil 50-54 caspase 3 Homo sapiens 56-65 11408917-11 2001 Furthermore, both active caspase-3 and apoptosis triggered by either ADR or 5-FU were inhibited significantly by the general caspase inhibitor Z-VAD-FMK, or a specific caspase-3 inhibitor DMQD-CHO. Fluorouracil 76-80 caspase 3 Homo sapiens 25-34 11408917-11 2001 Furthermore, both active caspase-3 and apoptosis triggered by either ADR or 5-FU were inhibited significantly by the general caspase inhibitor Z-VAD-FMK, or a specific caspase-3 inhibitor DMQD-CHO. Fluorouracil 76-80 caspase 3 Homo sapiens 168-177 10891390-6 2000 Finally, the activity of caspase-8 and caspase-3 showed a significant increase in response to 5-FU. Fluorouracil 94-98 caspase 3 Homo sapiens 39-48 10568827-0 1999 Apoptosis of colorectal adenocarcinoma induced by 5-FU and/or IFN-gamma through caspase 3 and caspase 8. Fluorouracil 50-54 caspase 3 Homo sapiens 80-89 10568827-3 1999 The activities of caspase 3 and caspase 8 increased when apoptosis was induced by 5-FU and/or IFN-gamma. Fluorouracil 82-86 caspase 3 Homo sapiens 18-27 10568827-6 1999 Thus, caspase 3 and caspase 8 play crucial roles in apoptosis induced by 5-FU and/or IFN-gamma, regardless of the Fas-Fas ligand system. Fluorouracil 73-77 caspase 3 Homo sapiens 6-15 33030957-8 2021 Knockout of PD-L1 was shown to attenuate the induction of DNA double-strand breaks (pH2AX) and caspase-3 cleavage by 5-fluorouracil (5-FU) and paclitaxel compared to parental CRC cells. Fluorouracil 117-131 caspase 3 Homo sapiens 95-104 33030957-8 2021 Knockout of PD-L1 was shown to attenuate the induction of DNA double-strand breaks (pH2AX) and caspase-3 cleavage by 5-fluorouracil (5-FU) and paclitaxel compared to parental CRC cells. Fluorouracil 133-137 caspase 3 Homo sapiens 95-104