PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 24738333-12 2014 Moreover, transcription and protein expression of bcl-2, NFKB, survivin, bax, p53 and caspase-3 of Raji cells were regulated at the most remarkable extent in ADM-As2O3, MNPs group as compared with other groups. Arsenic Trioxide 162-167 caspase 3 Homo sapiens 86-95 23980369-10 2013 HHT activated expressions of Caspase-3 and PARP in a dose dependent manner at 24 h. HHT at 40 ng/mL and ATO at 8.5 micromol/L could significantly activate expressions of Caspase-3 and Caspase-9, and down-regulate expressions of anti-apoptotic proteins Bcl-xl and Mcl-1. Arsenic Trioxide 104-107 caspase 3 Homo sapiens 29-38 23645216-5 2013 Cell cycle distribution, ROS level, and caspase-3 activation analyses suggest that AZT reduced the ATO-induced cytotoxic effect possibly via relative induction and diminution of cells accumulated in (G1, S) and (G2/M) phase, respectively, as well as through attenuation of ROS generation and subsequent caspase-3 inhibition. Arsenic Trioxide 99-102 caspase 3 Homo sapiens 40-49 23645216-5 2013 Cell cycle distribution, ROS level, and caspase-3 activation analyses suggest that AZT reduced the ATO-induced cytotoxic effect possibly via relative induction and diminution of cells accumulated in (G1, S) and (G2/M) phase, respectively, as well as through attenuation of ROS generation and subsequent caspase-3 inhibition. Arsenic Trioxide 99-102 caspase 3 Homo sapiens 303-312 24466103-3 2014 Here we show that ATO dose-dependently induces depolarization of mitochondrial inner transmembrane potential (DeltaPsim), up-regulation of Bax and down-regulation of Bcl-2 and Bcl-XL, caspase-3 activation, and phosphotidylserine (PS) exposure in platelets. Arsenic Trioxide 18-21 caspase 3 Homo sapiens 184-193 23980369-10 2013 HHT activated expressions of Caspase-3 and PARP in a dose dependent manner at 24 h. HHT at 40 ng/mL and ATO at 8.5 micromol/L could significantly activate expressions of Caspase-3 and Caspase-9, and down-regulate expressions of anti-apoptotic proteins Bcl-xl and Mcl-1. Arsenic Trioxide 104-107 caspase 3 Homo sapiens 170-179 24356076-7 2013 The expression of caspase-3 and Bax, which are targets of let-7d and miR-766, respectively, were up-regulated in As2O3 treated cells. Arsenic Trioxide 113-118 caspase 3 Homo sapiens 18-27 23363563-13 2013 CONCLUSION: Gen protects against the adverse cardiac effects of As2O3 partly by mitigating cardiomyocytes apoptosis induced by As2O3 through attenuating intracellular calcium overload and downregulating protein expression of p-JNK and pp38-MAPK to ameliorate the damage of Deltapsim leading to suppression of caspase-3 activation. Arsenic Trioxide 64-69 caspase 3 Homo sapiens 309-318 23363563-13 2013 CONCLUSION: Gen protects against the adverse cardiac effects of As2O3 partly by mitigating cardiomyocytes apoptosis induced by As2O3 through attenuating intracellular calcium overload and downregulating protein expression of p-JNK and pp38-MAPK to ameliorate the damage of Deltapsim leading to suppression of caspase-3 activation. Arsenic Trioxide 127-132 caspase 3 Homo sapiens 309-318 23373993-12 2013 These results suggest that ATO -induced apoptosis in retinoblastoma cells is part mediated by decreasing expression of miR-376a, which subsequently increased caspase-3 expression. Arsenic Trioxide 27-30 caspase 3 Homo sapiens 158-167 22922937-7 2012 ATO and sulforaphane co-treatment augmented apoptotic induction as demonstrated by cleavage of caspase-3, -4 and PARP. Arsenic Trioxide 0-3 caspase 3 Homo sapiens 107-120 23404534-6 2013 It was also observed that apoptosis occurred through activation of caspase-3 and phosphatidylserine externalization in human hepatocellular carcinoma cells exposed to arsenic trioxide. Arsenic Trioxide 167-183 caspase 3 Homo sapiens 67-76 22391177-5 2012 Compared with the group treated with As(2)O(3) (10 micromol/L) alone, zVAD-fmk (20 micromol/L) combined with As(2)O(3) (10 micromol/L) treatment group showed significant increase of expressions of Caspase-3 and BCL-2. Arsenic Trioxide 109-118 caspase 3 Homo sapiens 197-206 22931643-5 2012 It is concluded that HBO combined with As(2)O(3) can increase the expression of caspase 3 mRNA and decrease the expression of HIF-1a and VEGF mRNA, which may be one of molecular mechanisms underlying their synergistic antileukemia efficacy. Arsenic Trioxide 39-48 caspase 3 Homo sapiens 80-89 22072212-3 2012 The apoptotic effects of ATO on the NB4 cell line at a pharmacological dose (2 muM) was verified using cell growth and viability assays, MTT assay, BrdU cell proliferation assay, flow cytometric analysis, and caspase-3 activity assay. Arsenic Trioxide 25-28 caspase 3 Homo sapiens 209-218 21502917-10 2011 The results showed that the growth inhibitory and apoptotic effects of As2O3 and AZT on human hepatoma cells could be related to the inhibition of telomerase and the activation of caspase 3. Arsenic Trioxide 71-76 caspase 3 Homo sapiens 180-189 21826188-6 2012 The ATO/CMEMM-induced activation of caspase-3 and caspase-9 can be blocked by NAC. Arsenic Trioxide 4-7 caspase 3 Homo sapiens 36-45 21846841-5 2011 11,12-EET also prevented the ATO-induced activation of p38 mitogen-activated protein kinase, c-Jun NH(2)-terminal kinase, caspase-3, and caspase-9. Arsenic Trioxide 29-32 caspase 3 Homo sapiens 122-131 22977528-0 2011 Arsenic trioxide induces the apoptosis of human breast cancer MCF-7 cells through activation of caspase-3 and inhibition of HERG channels. Arsenic Trioxide 0-16 caspase 3 Homo sapiens 96-105 22977528-8 2011 Taken together, the results indicate that arsenic trioxide induces the apoptosis of human breast cancer MCF-7 cells at least in part through the activation of caspase-3 and the decrease in HERG expression. Arsenic Trioxide 42-58 caspase 3 Homo sapiens 159-168 21518486-3 2011 The results showed that the bortezomib combined with As(2)O(3) could induce significant apoptosis of NB4 cells and activation of caspase 3 and caspase 9, but As(2)O(3) (0.5 micromol/L) alone could not cause marked activation of caspase cascade and apoptosis of NB4 cells. Arsenic Trioxide 53-62 caspase 3 Homo sapiens 129-138 21518486-4 2011 The expression level of NOXA in NB4 cells induced by bortezomib combined with As(2)O(3) was up-regulated; the activation level of caspase-3 and apoptotic rate of NB4 cells treated by bortezomib combined with As(2)O(3) decreased after specifically silencing the NOXA gene. Arsenic Trioxide 78-87 caspase 3 Homo sapiens 130-139 20723293-8 2010 The STI571 combined with As2O3 can enhance these two effects, increase the expression of caspase-3 mRNA and decrease the expression of bcl-xL mRNA. Arsenic Trioxide 25-30 caspase 3 Homo sapiens 89-98 21655183-4 2011 Our data demonstrated that ATO induced cell apoptosis by decreasing levels of phosphorylated AKT (p-AKT) and activating caspase-3 and caspase-9. Arsenic Trioxide 27-30 caspase 3 Homo sapiens 120-129 21655183-8 2011 Moreover, the activation of caspase-3 by ATO treatment improved AKT dephosphorylation, not only by cleaving the regulatory A subunit of protein phosphatase 2A (PP2A), but also by increasing its activation. Arsenic Trioxide 41-44 caspase 3 Homo sapiens 28-37 20796291-11 2010 CONCLUSION: Taken together, our research demonstrated that ATO represents an apoptosis-inducing agent and its apoptotic mechanisms involve phosphatidylserine externalization, caspase 3 activation and nucleosomal DNA fragmentation. Arsenic Trioxide 59-62 caspase 3 Homo sapiens 175-184 20799280-4 2011 As2O3 induced apoptosis of NCI-H2052 cells, which was accompanied by activation of c-Jun NH2-terminal kinase (JNK)1/2, extracellular signal-regulated kinase (ERK)1/2, and caspase-3. Arsenic Trioxide 0-5 caspase 3 Homo sapiens 171-180 20799280-5 2011 zVAD-fmk, a broad-spectrum caspase inhibitor, inhibited As2O3-induced apoptosis and activation of caspase-3, but not that of JNK1/2 and ERK1/2. Arsenic Trioxide 56-61 caspase 3 Homo sapiens 98-107 20799280-6 2011 Small interfering RNAs (siRNAs) targeting JNK1/2 suppressed As2O3-induced caspase-3 activation and apoptosis, indicating that JNK1/2 regulate As2O3-induced apoptosis though caspase cascade. Arsenic Trioxide 60-65 caspase 3 Homo sapiens 74-83 20799280-6 2011 Small interfering RNAs (siRNAs) targeting JNK1/2 suppressed As2O3-induced caspase-3 activation and apoptosis, indicating that JNK1/2 regulate As2O3-induced apoptosis though caspase cascade. Arsenic Trioxide 142-147 caspase 3 Homo sapiens 74-83 20724260-6 2010 RESULTS: It was showed that KNK437 (HSPs inhibitor) or HSF1 knockdown significantly enhanced cell death, MMP disruption, JNK phosphorylation and caspase-3 cleavage induced by ATO, which was accompanied by abrogation of HSPs induction, while heat pre-treatment with clear HSPs induction had strong protection on the effects mentioned above. Arsenic Trioxide 175-178 caspase 3 Homo sapiens 145-154 20723293-9 2010 Therefore, the effect of STI571 combined with As2O3 on expression of caspase 3 and bcl-xL mRNA may be one of molecular mechanisms underlying their synergic antileukemia efficacy. Arsenic Trioxide 46-51 caspase 3 Homo sapiens 69-78 20632473-8 2010 Furthermore, arsenic trioxide modulated caspase 3 activity and induced p38 MAP kinase activation in A549 cells. Arsenic Trioxide 13-29 caspase 3 Homo sapiens 40-49 20454603-13 2010 Our findings revealed that arsenic trioxide modulated caspase 3 activity and induced p38 map kinase activation in lung carcinoma (A549) cells. Arsenic Trioxide 27-43 caspase 3 Homo sapiens 54-63 19664237-15 2009 The expression of caspase-3 in cells treated with the combination of As2O3 and DDP did not differ from that in cells treated with a single agent. Arsenic Trioxide 69-74 caspase 3 Homo sapiens 18-27 18599993-4 2008 The activation of caspase-3 was increased, and the rate of bcl-2/bax was down-regulated in the HXO-RB(44) cells processed with arsenic trioxide. Arsenic Trioxide 127-143 caspase 3 Homo sapiens 18-27 18566239-8 2008 We show that As2O3 decreases AKT protein via caspase-mediated degradation, abrogated by caspase-6, caspase-8, caspase-9, and caspase-3 inhibitors but not proteosome inhibitors. Arsenic Trioxide 13-18 caspase 3 Homo sapiens 125-134 19322013-7 2009 RESULTS: ATO inhibited proliferation and induced apoptosis of T24 cells in a dose-dependent manner, caused an increase of percentage of cells in the G(1) phase and a decrease in the S and G(2) phases, and upregulated the expression of activated caspase-3 and reduced PKC activity. Arsenic Trioxide 9-12 caspase 3 Homo sapiens 245-254 17956674-7 2007 After treating U266 cells with 2 micromol/L As2O3 at different time points, a time-dependent reduction of procaspase-3, hTERT mRNA and protein was found without any change of bcl-2 expression. Arsenic Trioxide 44-49 caspase 3 Homo sapiens 106-118 18158874-10 2008 Following As2O3, lysosomes were activated as indicated by increased levels of cathepsins B and L. The apoptotic response of HL60 cells to As2O3 was suggested by the collapse of mitochondrial membrane potential, release of cytochrome c from mitochondria, and the activation of caspase-3. Arsenic Trioxide 138-143 caspase 3 Homo sapiens 276-285 17956674-8 2007 It is concluded that the As2O3 can change the mitochondrial transmembrane potential, initiating the mitochondial apoptosis pathway, leading in turn to caspase-3 activation, and inducing the apoptosis of U266 cells. Arsenic Trioxide 25-30 caspase 3 Homo sapiens 151-160 17531122-13 2007 CONCLUSIONS: Berbamine induces caspase-3-dependent apoptosis of leukemia NB4 cells via survivin-mediated pathway, suggesting that berbamine may be a novel potential agent against APL with a mechanism distinct from that of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). Arsenic Trioxide 257-273 caspase 3 Homo sapiens 31-40 17495969-4 2007 The results showed that cotreatment of bortezomib at 32 nM, a half concentration for growth arrest, and ATO at 1 microM, a dose with no significant cytotoxic effect, synergistically induced apoptosis in the cell line, followed by enhanced mitochondrial dysfunction, release of cytochrome c and apoptosis-inducing factor, caspase-3 cleavage and degradation of poly-adenosine diphosphate-ribose polymerase together with the decreased Bcr-Abl protein. Arsenic Trioxide 104-107 caspase 3 Homo sapiens 321-330 17531122-13 2007 CONCLUSIONS: Berbamine induces caspase-3-dependent apoptosis of leukemia NB4 cells via survivin-mediated pathway, suggesting that berbamine may be a novel potential agent against APL with a mechanism distinct from that of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). Arsenic Trioxide 275-278 caspase 3 Homo sapiens 31-40 16685442-4 2006 In addition, combination treatment with As2O3 and sulindac increased the catalytic activity of caspase-3, -8, and -9 along with induction of Fas/FasL expression and cytosolic release of cytochrome c. Arsenic Trioxide 40-45 caspase 3 Homo sapiens 95-116 16010437-4 2005 Our data demonstrated that ATO is a potent agent against AMKL as indicated by apoptotic markers, Annexin V and caspase-3. Arsenic Trioxide 27-30 caspase 3 Homo sapiens 111-120 15979894-7 2005 CASPASE-3 activity was also enhanced after As(2)O(3) treatment. Arsenic Trioxide 43-52 caspase 3 Homo sapiens 0-9 15665116-4 2005 The potentiation of As2O3-provoked apoptosis involved the increased disruption of mitochondrial transmembrane potential, increased caspase-3 activation and cytochrome c release from mitochondria, increased Bax and Bid activation, and attenuation of 27-kDa heat shock protein (HSP27) expression; the potentiation was prevented by Bcl-2 overexpression. Arsenic Trioxide 20-25 caspase 3 Homo sapiens 131-140 15493360-7 2004 Western blot analysis revealed activation of caspase -3, -7, and -9 by arsenic trioxide. Arsenic Trioxide 71-87 caspase 3 Homo sapiens 45-67 16051535-6 2005 Expression of activated caspase 3 in HeLa cells also indicates that the C-terminal 16 residues are important for mdb3-mediated apoptosis in cells treated with As2O3. Arsenic Trioxide 159-164 caspase 3 Homo sapiens 24-33 15637062-4 2005 Overexpression of PRAM-1 in the NB4 APL cell line increased arsenic trioxide-induced JNK activation through a caspase 3-like-dependent activity. Arsenic Trioxide 60-76 caspase 3 Homo sapiens 110-119 15637062-5 2005 Dissociation of the SH3 domain from the rest of the HIP-55 protein was observed in the NB4 APL cell line treated with arsenic trioxide due to specific cleavage by caspase 3-like enzymes. Arsenic Trioxide 118-134 caspase 3 Homo sapiens 163-172 15637062-7 2005 Taken together, our results suggest that the caspase 3-cleaved SH3 domain of HIP-55 is likely involved in PRAM-1-mediated JNK activation upon arsenic trioxide-induced differentiation of NB4 cells. Arsenic Trioxide 142-158 caspase 3 Homo sapiens 45-54 14668793-7 2003 IFNgamma boosted As2O3-induced apoptosis in APL cells as tested by TUNEL, Annexin V staining and activation of caspase 3. Arsenic Trioxide 17-22 caspase 3 Homo sapiens 111-120 14559676-6 2003 As2O3-induced apoptosis was accompanied by down-regulation of Bcl-xL protein expression and activation of apoptosis protein caspase-3, as identified by Western blotting. Arsenic Trioxide 0-5 caspase 3 Homo sapiens 124-133 12931215-3 2003 Apoptosis induced by 1 microM of As(2)O(3) in NKM-1 cells was accompanied by an increased cellular content of H(2)O(2), a decreased mitochondrial membrane potential (Deltapsim), and activation of caspase-3. Arsenic Trioxide 33-42 caspase 3 Homo sapiens 196-205 14559676-7 2003 CONCLUSION: As2O3 exerts apoptosis-inducing effects on human Burkitt lymphoma cells through down-regulation of Bcl-xL protein expression and activation of apoptosis protein caspase-3, and may serve as a candidate therapeutic agent against malignant lymphoma for both systemic and local therapies. Arsenic Trioxide 12-17 caspase 3 Homo sapiens 173-182 12750841-0 2003 Arsenic trioxide induces apoptosis in cells of MOLT-4 and its daunorubicin-resistant cell line via depletion of intracellular glutathione, disruption of mitochondrial membrane potential and activation of caspase-3. Arsenic Trioxide 0-16 caspase 3 Homo sapiens 204-213 12963972-2 2003 As4O6 induced apoptosis in U937 leukemic cells at much lower concentrations than As2O3 via an early increase of cellular reactive oxygen species (ROS), and a decrease in cellular mitochondrial membrane potential, followed by cytochrome c release and caspase-3 activation. Arsenic Trioxide 0-5 caspase 3 Homo sapiens 250-259 12963972-3 2003 As4O6 generated ROS and induced caspase-3 activation more potently than As2O3 in U937 cells. Arsenic Trioxide 0-5 caspase 3 Homo sapiens 32-41 14632209-6 2003 As2O3-induced Sezary cell death involves activation of caspase-3, cleavage of poly(ADP-ribose)polymerase, and cytochrome c release, but was only partially inhibited by the pancaspase inhibitor Z-VAD.fluoromethylketone. Arsenic Trioxide 0-5 caspase 3 Homo sapiens 55-64 12750841-12 2003 Clinically relevant doses of AA enhanced the anticancer effects of As(2)O(3) via the disruption of MMP, activation of caspase-3, and induction of apoptosis. Arsenic Trioxide 67-76 caspase 3 Homo sapiens 118-127 12760770-15 2003 Activation of the caspase-3 proteolytic pathway may be one of the pivotal ways of apoptosis procedure induced by arsenic trioxide. Arsenic Trioxide 113-129 caspase 3 Homo sapiens 18-27 12883267-3 2003 The results show the caspase-3, caspase-7, and caspase-9 are all activated by arsenic trioxide, together with cleavage of the downstream caspase-3 target poly ADP ribose polymerase (PARP). Arsenic Trioxide 78-94 caspase 3 Homo sapiens 21-30 12883267-3 2003 The results show the caspase-3, caspase-7, and caspase-9 are all activated by arsenic trioxide, together with cleavage of the downstream caspase-3 target poly ADP ribose polymerase (PARP). Arsenic Trioxide 78-94 caspase 3 Homo sapiens 137-146 12754411-4 2003 When treated with micromolar concentrations of As(2)O(3), HepG2 cells became highly apoptotic paralleled with activation of caspase-3 and members of mitogen-activated protein kinases (MAPKs) including extracellular signal-regulated kinase (ERK) and c-jun NH(2)-terminal kinase (JNK) but not p38 MAP kinase. Arsenic Trioxide 47-56 caspase 3 Homo sapiens 124-133 12754411-6 2003 Addition of n-acetyl cysteine (NAC) or diphenyleneiodonium (DPI) effectively protected cells from apoptosis and significantly lowered As(2)O(3)-induced activation of caspase-3. Arsenic Trioxide 134-143 caspase 3 Homo sapiens 166-175 12168106-3 2002 Arsenic trioxide treatment of U937 cells leads to apoptosis, which is accompanied by activation of caspase 3 (as measured by decreased levels of the 32 kDa inactive form and increased proteolytic cleavage of PLC-gamma1). Arsenic Trioxide 0-16 caspase 3 Homo sapiens 99-108 12168106-6 2002 Bcl-2 overexpression attenuates arsenic trioxide-induced apoptosis in U937 cells by inhibition of caspase 3 activity, but not inhibition of Akt. Arsenic Trioxide 32-48 caspase 3 Homo sapiens 98-107 12063550-3 2002 The cells underwent apoptosis in response to As2O3, accompanied by a decrease of mitochondrial membrane potential and caspase-3 activation. Arsenic Trioxide 45-50 caspase 3 Homo sapiens 118-127 26680881-6 2002 As2O3 increased the catalytic activity of caspase family cysteine proteases including caspase-3 and -9 proteases. Arsenic Trioxide 0-5 caspase 3 Homo sapiens 86-102 12174905-8 2002 Furthermore, Western blotting analysis indicated that caspase-3 was activated following arsenic trioxide as measured by procaspase-3 cleavage and PARP cleavage. Arsenic Trioxide 88-104 caspase 3 Homo sapiens 54-63 12174905-8 2002 Furthermore, Western blotting analysis indicated that caspase-3 was activated following arsenic trioxide as measured by procaspase-3 cleavage and PARP cleavage. Arsenic Trioxide 88-104 caspase 3 Homo sapiens 120-132 12063550-7 2002 The above results indicate that the induction of HeLa cell apoptosis by As2O3 involved an early decrease in cellular mitochondrial membrane potential and increase in ROS content, predominantly H2O2, followed by caspase-3 activation and DNA fragmentation. Arsenic Trioxide 72-77 caspase 3 Homo sapiens 211-220 12034346-4 2002 The mechanistic study showed that 2 microM of As(2)O(3) acted through induction of apoptosis in which caspase-3 was activated. Arsenic Trioxide 46-55 caspase 3 Homo sapiens 102-111 12023044-5 2002 Apoptosis of the cells by combined treatment of As2O3 and radiation was associated with reactive oxygen species generation and loss of mitochondrial membrane potential, resulting in the activation of caspase-9 and caspase-3. Arsenic Trioxide 48-53 caspase 3 Homo sapiens 214-223 12148893-4 2002 Activation of caspases 3, 8, and 9, loss of mitochondrial transmembrane potential and cleavage of poly (adenosine diphosphate-ribose) polymerase (PARP) were observed during As2O3 treatment. Arsenic Trioxide 173-178 caspase 3 Homo sapiens 14-34 11739184-0 2001 Arsenic trioxide induces apoptosis in human T-cell leukemia virus type 1- and type 2-infected cells by a caspase-3-dependent mechanism involving Bcl-2 cleavage. Arsenic Trioxide 0-16 caspase 3 Homo sapiens 105-114 12005185-8 2002 All these findings indicate that arsenic trioxide-induced apoptosis in SW480 cells is executed by the activation of caspase 3 without mediating by mitochondria under the overproduction of reactive oxygen species. Arsenic Trioxide 33-49 caspase 3 Homo sapiens 116-125 11866444-2 2002 HLE cells underwent apoptosis at 2 microM ATO, which was executed by the activation of caspase-3 through the mitochondrial pathway mediated by caspase-8 activation and Bid truncation. Arsenic Trioxide 42-45 caspase 3 Homo sapiens 87-96 10673743-3 2000 1.0 microM As2O3-induced apoptosis was associated with condensation of the mitochondrial matrix, disruption of mitochondrial transmembrane potentials (DeltaPsim) and activation of caspase-3 in acute promyelocytic leukemia (APL) cells regardless of their sensitivity to all-trans retinoic acid (ATRA). Arsenic Trioxide 11-16 caspase 3 Homo sapiens 180-189 11172589-0 2001 Potential role of caspase-3 and -9 in arsenic trioxide-mediated apoptosis in PCI-1 head and neck cancer cells. Arsenic Trioxide 38-54 caspase 3 Homo sapiens 18-34 11172589-11 2001 These results suggest that apoptosis of PCI-1 cells by As2O3 is induced by activation of caspase-3 via cytochrome c, caspase-9 and Apaf-1 complex. Arsenic Trioxide 55-60 caspase 3 Homo sapiens 89-98 11146441-0 2001 Arsenic trioxide induces apoptosis in human gastric cancer cells through up-regulation of p53 and activation of caspase-3. Arsenic Trioxide 0-16 caspase 3 Homo sapiens 112-121 11779429-0 2001 Arsenic trioxide induces multiple myeloma cell apoptosis via disruption of mitochondrial transmembrane potentials and activation of caspase-3. Arsenic Trioxide 0-16 caspase 3 Homo sapiens 132-141 11779429-7 2001 As2O3-induced apoptosis was accompanied by mitochondrial transmembrane potentials (delta psi m) collapse and caspase-3 activation in the presence of intact membrane. Arsenic Trioxide 0-5 caspase 3 Homo sapiens 109-118 11021749-6 2000 Treatment with 1 microM As2O3 induced the activation of caspase 3 as well as a loss of mitochondrial transmembrane potential (deltapsim) in NB4 but not in NB4/As. Arsenic Trioxide 24-29 caspase 3 Homo sapiens 56-65 11520058-0 2001 Arsenic trioxide induces G2/M growth arrest and apoptosis after caspase-3 activation and bcl-2 phosphorylation in promonocytic U937 cells. Arsenic Trioxide 0-16 caspase 3 Homo sapiens 64-73 11454688-8 2001 As2O3 activated p38, JNK, and caspase-3 dose dependently. Arsenic Trioxide 0-5 caspase 3 Homo sapiens 30-39 9801394-9 1998 Arsenic trioxide induced the expression of the proenzymes of caspase 2 and caspase 3 and activation of both caspase 1 and caspase 3. Arsenic Trioxide 0-16 caspase 3 Homo sapiens 75-84 10477740-11 1999 The induction of apoptosis by As(2)O(3) involves an early decrease in cellular mitochondrial membrane potential and increase in H(2)O(2) content, followed by cytochrome c release, caspase 3 activation, DNA fragmentation, and the classic morphologic changes of apoptosis. Arsenic Trioxide 30-39 caspase 3 Homo sapiens 180-189 10428472-0 1999 Arsenic trioxide induces apoptosis in neuroblastoma cell lines through the activation of caspase 3 in vitro. Arsenic Trioxide 0-16 caspase 3 Homo sapiens 89-98 10428472-3 1999 As2O3-induced apoptosis in neuroblastoma cells was shown to occur through the activation of caspase 3, as judged from Western blot analysis and apoptosis inhibition assay. Arsenic Trioxide 0-5 caspase 3 Homo sapiens 92-101 9801394-9 1998 Arsenic trioxide induced the expression of the proenzymes of caspase 2 and caspase 3 and activation of both caspase 1 and caspase 3. Arsenic Trioxide 0-16 caspase 3 Homo sapiens 122-131 30333888-6 2018 Western blot analysis revealed that ATO treatment affected the expression of apoptosis-associated proteins by downregulating the anti-apoptotic protein B-cell lymphoma-2 (Bcl-2) and upregulating the pro-apoptotic protein Bcl-2-associatedX and the degree of caspase-3 cleavage. Arsenic Trioxide 36-39 caspase 3 Homo sapiens 257-266 31079498-8 2019 Overexpression of Id-1 could attenuate the inhibition or promotion of As2O3 on proliferation, apoptosis and Caspase-3, Bax and Bcl-2 protein expression in Tca8113 cells. Arsenic Trioxide 70-75 caspase 3 Homo sapiens 108-117 31257975-6 2019 As2O3 and As4O6 treatment induced caspase-3-dependent apoptosis in all cell lines compared to the respective control groups (p < .05). Arsenic Trioxide 0-5 caspase 3 Homo sapiens 34-43 31257975-6 2019 As2O3 and As4O6 treatment induced caspase-3-dependent apoptosis in all cell lines compared to the respective control groups (p < .05). Arsenic Trioxide 10-15 caspase 3 Homo sapiens 34-43 30316766-5 2018 Moreover, we found that the positive regulatory role of the PI3K inhibition in augmenting the intracellular level of reactive oxygen species disturbed the balance between the death promoter and death repressor genes, which in turn amplified the caspase-3-dependent apoptotic activity of ATO in NB4. Arsenic Trioxide 287-290 caspase 3 Homo sapiens 245-254 29164574-12 2017 CONCLUSIONS: As2O3 can inhibit proliferation of glioma cells and induce its apoptosis, which may be correlated with down-regulation of expressions of apoptosis-related factors, Fas, FasL and Bax, and apoptosis-related proteins, p53, caspase-3 and caspase-9. Arsenic Trioxide 13-18 caspase 3 Homo sapiens 233-242 30213730-4 2018 ATO-induced apoptosis in U937 cells was characterized by activation of caspase-3/-9, mitochondrial depolarization, and MCL1 downregulation. Arsenic Trioxide 0-3 caspase 3 Homo sapiens 71-83 29910624-11 2018 Conclusion: The present results show that AZT could increase the sensitization of As2O3 for inhibiting proliferation and promoting apoptosis of HepG2 cells through regulating the expression of Egr-1, which may control the expression of p53 and caspase-3. Arsenic Trioxide 82-87 caspase 3 Homo sapiens 244-253 30343279-8 2018 The intracellular mechanisms of cytotoxicity of As2O3 plus resveratrol were revealed as ROS accumulation and relative decrease of MMP, leading to activation of caspase-3 and -9, but not of caspase-1, -7 and-8. Arsenic Trioxide 48-53 caspase 3 Homo sapiens 160-176 27592447-8 2016 Experiments using inhibitors of antioxidant enzymes in the presence of arsenic trioxide-treated osteoblasts demonstrated that glutathione and superoxide dismutase were responsible for reducing oxidative stress, caspase-3 activity, and apoptosis and that heat shock proteins helped reduce caspase-3 activity. Arsenic Trioxide 71-87 caspase 3 Homo sapiens 211-220 28823259-6 2017 CONCLUSION: Arsenic trioxide combined with itraconazole can inhibit the KG1a cell proliferation and induce apoptosis, which may be related with the inhibition of Hh signaling pathway and upregulation of both Caspase-3 and BAX protein expression, and provided experimental data of arsenic trioxide combined with itraconazole for the treatment of refractory AML. Arsenic Trioxide 12-28 caspase 3 Homo sapiens 208-217 28966729-12 2017 Western blot data showed that ATO upregulated the expression of caspase 3, Bax, and cytochrome C, and down-regulated the expression of Bcl-2. Arsenic Trioxide 30-33 caspase 3 Homo sapiens 64-73 27592447-8 2016 Experiments using inhibitors of antioxidant enzymes in the presence of arsenic trioxide-treated osteoblasts demonstrated that glutathione and superoxide dismutase were responsible for reducing oxidative stress, caspase-3 activity, and apoptosis and that heat shock proteins helped reduce caspase-3 activity. Arsenic Trioxide 71-87 caspase 3 Homo sapiens 288-297 25258189-7 2016 The caspase-9 and caspase-3 activities were time-dependently increased in arsenic trioxide-treated HUMSC and HMSC-bm. Arsenic Trioxide 74-90 caspase 3 Homo sapiens 18-27 24944602-6 2014 In addition, ATO significantly decreased the expression of antiapoptotic proteins, B-cell lymphoma 2 (Bcl-2) and B cell lymphoma-extra large (Bcl-xL), but markedly increased the expression of proapoptotic proteins, including c-Jun N-terminal kinase (JNK), phosphorylated-JNK, Bax, full length caspase-3 and cleaved caspase-3. Arsenic Trioxide 13-16 caspase 3 Homo sapiens 293-302 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. Arsenic Trioxide 13-18 caspase 3 Homo sapiens 83-92 25415199-2 2014 As2O3 induced this two cell lines apoptosis via activation of caspase-3/8 and cleavage of poly (ADP-ribose) polymerase (PARP), a DNA repair enzyme. Arsenic Trioxide 0-5 caspase 3 Homo sapiens 62-118 25415199-7 2014 Our findings suggest that As2O3 may induce apoptosis in MUTZ-1 and SKM-1 cells by two independent pathways: first, by activation of caspase-3/8 and PARP; and second, by inhibition of NF-kappaB activity, which results in downregulation of hTERT expression. Arsenic Trioxide 26-31 caspase 3 Homo sapiens 132-143 24815320-0 2014 cAMP protects acute promyelocytic leukemia cells from arsenic trioxide-induced caspase-3 activation and apoptosis. Arsenic Trioxide 54-70 caspase 3 Homo sapiens 79-88 25128771-8 2014 And, high dose of ATO increased Bax/Bcl-2 ratio in a time-dependent fashion and activated caspase-3 apoptotic signaling. Arsenic Trioxide 18-21 caspase 3 Homo sapiens 90-99 24944602-6 2014 In addition, ATO significantly decreased the expression of antiapoptotic proteins, B-cell lymphoma 2 (Bcl-2) and B cell lymphoma-extra large (Bcl-xL), but markedly increased the expression of proapoptotic proteins, including c-Jun N-terminal kinase (JNK), phosphorylated-JNK, Bax, full length caspase-3 and cleaved caspase-3. Arsenic Trioxide 13-16 caspase 3 Homo sapiens 315-324 24944602-7 2014 These results indicated that ATO inhibited the proliferation and induced apoptosis in THP1 cells partially via blocking the inhibitory effects of EVI-1 on the JNK signaling pathway with the involvement of apoptosis-associated proteins, including Bax, Bcl-2, Bcl-xL and caspase-3. Arsenic Trioxide 29-32 caspase 3 Homo sapiens 269-278 24482137-5 2014 As2O3 activated caspase-3 and -9, and PARP cleavage in a dose-dependent manner. Arsenic Trioxide 0-5 caspase 3 Homo sapiens 16-32 24599717-10 2014 Compared to mono-therapy, ATO/CDDP combinatorial therapy significantly augmented the loss of mitochondrial potential, caspase-3/7 activity and subsequent apoptosis. Arsenic Trioxide 26-29 caspase 3 Homo sapiens 118-127