PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 20132660-5 2010 We have shown that nilotinib induces apoptosis in imatinib-resistant K562 CML cells which have the wild-type BCR-ABL fusion gene almost to the same extent as it does in the parental sensitive cells by the increase in caspase-3 enzyme activity and the decrease in mitochondrial membrane potential. Imatinib Mesylate 50-58 caspase 3 Homo sapiens 217-226 20307198-0 2010 Combination of fludarabine and imatinib induces apoptosis synergistically through loss of mitochondrial membrane potential and increases in caspase-3 enzyme activity in human K562 chronic myleloid leukemia cells. Imatinib Mesylate 31-39 caspase 3 Homo sapiens 140-149 20094798-5 2010 Nutlin-3 and imatinib synergistically induced Bax activation, mitochondrial membrane depolarization, and caspase-3 cleavage leading to caspase-dependent apoptosis, which was inhibited by overexpression of Bcl-XL. Imatinib Mesylate 13-21 caspase 3 Homo sapiens 105-114 20094798-7 2010 Furthermore, activation of Bax as well as caspase-3 induced by combined treatment with imatinib and nutlin-3 was observed preferentially in cells expressing p21 at reduced levels. Imatinib Mesylate 87-95 caspase 3 Homo sapiens 42-51 20031210-6 2010 An increased level of cleaved PARP and decreased level of pro-caspase 3 were noted when K562/FLT3-siRNA cells were treated with imatinib. Imatinib Mesylate 128-136 caspase 3 Homo sapiens 58-71 20723293-0 2010 [Effects of STI571 combined with As2O3 on proliferation, apoptosis and caspase 3, Bcl-xL expression of K562 cells]. Imatinib Mesylate 12-18 caspase 3 Homo sapiens 71-80 20723293-1 2010 This study was aimed to explore the effects of STI571 alone or with As2O3 on proliferation, apoptosis and caspase 3, bcl-xL mRNA expression of K562 cells, and the molecular mechanism of As2O3 enhancing the anti-leukemia effect of STI571 so as to provide the scientific basis for clinical treatment of chronic myeloid leukemia. Imatinib Mesylate 47-53 caspase 3 Homo sapiens 106-115 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. Imatinib Mesylate 4-10 caspase 3 Homo sapiens 89-98 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. Imatinib Mesylate 25-31 caspase 3 Homo sapiens 69-78 19340007-9 2009 LynDeltaN also inhibits imatinib-mediated caspase-3 activation in the small proportion of nilotinib-resistant K562 cells overexpressing Lyn that can engage an apoptotic program upon imatinib stimulation. Imatinib Mesylate 24-32 caspase 3 Homo sapiens 42-51 19058199-8 2009 Low-dose imatinib was synergistic in combination with doxorubicin and caused increased G2/M- and S-phase arrest and apoptosis as evidenced by enhanced caspase-3 activation and sub-G1 DNA accumulation. Imatinib Mesylate 9-17 caspase 3 Homo sapiens 151-160 19490758-7 2009 Imatinib and docetaxel induced apoptosis through caspase-3 enzyme activity and mitochondrial membrane potential. Imatinib Mesylate 0-8 caspase 3 Homo sapiens 49-58 18401414-5 2008 Overexpression of SphK1 in LAMA84-s cells impaired apoptosis and inhibited the effects of imatinib on caspase-3 activation, cytochrome c and Smac release from mitochondria through modulation of Bim, Bcl-xL and Mcl-1 expression. Imatinib Mesylate 90-98 caspase 3 Homo sapiens 102-111 18843975-5 2008 Annexin V/PI staining and DNA ladder indicated that Imatinib had a substantial effect on inducing apoptosis of KM3 cells in a dose-dependent manner and induced pro-caspase-3 and poly ADP-ribose polymerase (PARP) cleaved. Imatinib Mesylate 52-60 caspase 3 Homo sapiens 160-173 15770664-4 2005 In JURL-MK1 cells, the apoptosis is faster in comparison with K562 cells: the caspase-3 activity reaches the peak value (20 to 30 fold of the control) after about 40 h and the apoptosis proceeds to its culmination point, the DNA fragmentation, within 48 h following 1 microM Imatinib addition. Imatinib Mesylate 275-283 caspase 3 Homo sapiens 78-87 16596277-3 2006 In these cells, STI571 induced pro-caspase-12 or pro-caspase-7 cleavage and it affected caspase-3 activity and induced the endoplasmic reticulum (ER)-resident chaperone, glucose-regulated protein 78. Imatinib Mesylate 16-22 caspase 3 Homo sapiens 88-97 17926190-7 2007 Enhanced apoptosis, cytochrome C release, and caspase 3 cleavage as well as noticeable decrease of Mcl-1 and Bcl-XL were observed in K562 cells treated with both (-)gossypol and imatinib. Imatinib Mesylate 178-186 caspase 3 Homo sapiens 46-55 12850478-6 2003 In addition, caspase-3 was activated by treatment of cells with STI571 and LY294002 but not with PD98059. Imatinib Mesylate 64-70 caspase 3 Homo sapiens 13-22 15657060-5 2005 Moreover, inhibition of c-Abl with STI571 blocked DNA damage-induced autoprocessing of caspase-9 to the p35 subunit and activation of caspase-3. Imatinib Mesylate 35-41 caspase 3 Homo sapiens 134-143 12850478-8 2003 Primary leukemia cells from patients with CML blast crisis did not show inhibition of ERK1/2 or Akt kinase activity and were resistant to caspase-3-associated apoptosis after treatment with STI571. Imatinib Mesylate 190-196 caspase 3 Homo sapiens 138-147 34781823-7 2021 Secondly, cell proliferation of imatinib-resistant renal cell carcinoma cells was suppressed by PDIA6 silencing, and the apoptosis was promoted with reduced Bcl-2, enhanced Bax and cleaved caspase-3. Imatinib Mesylate 32-40 caspase 3 Homo sapiens 189-198 11782377-4 2002 Cells exposed to STI571 in combination with PD184352 for 48 h demonstrated a very dramatic increase in mitochondrial dysfunction (e.g., loss of DeltaPsim and cytosolic cytochrome c release) associated with procaspase-3 activation, poly(ADP-ribose) polymerase cleavage, and the appearance of the characteristic morphological features of apoptosis. Imatinib Mesylate 17-23 caspase 3 Homo sapiens 206-218 12231544-3 2002 RESULTS: In K562 cells, coadministration of marginally toxic concentrations of STI571 (200 nM) and flavopiridol (150 nM) for 48 h resulted in a marked increase in mitochondrial damage (e.g., cytochrome c release), activation of caspase-3, caspase-8, and Bid, and apoptosis. Imatinib Mesylate 79-85 caspase 3 Homo sapiens 228-237 12021410-5 2002 The results further show that STI571 inhibits ara-C-induced loss of mitochondrial transmembrane potential, caspase-3 activation, and apoptosis. Imatinib Mesylate 30-36 caspase 3 Homo sapiens 107-116 12411057-6 2002 Caspase-3 was activated and there was an cytosolic accumulation of cyto C. CONCLUSION: STI571 could rapidly decrease the tyrosine phosphorylation level of P210(BCR/ABL). Imatinib Mesylate 87-93 caspase 3 Homo sapiens 0-9 11179439-6 2001 Use of the Bcr-Abl tyrosine kinase inhibitor STI-571 resulted in a reduction in Bcl-xL levels and potentiation of dexrazoxane-induced apoptosis related to an earlier onset and more extensive cleavage of caspase-3. Imatinib Mesylate 45-52 caspase 3 Homo sapiens 203-212 33022360-9 2020 Restoration of physiological apoptosis by increasing the release of intracellular calcium to generate ROS thereby reducing the mitochondrial membrane potential for the release of cytochrome c and activation of caspase-3 was also reported with Imatinib administration. Imatinib Mesylate 243-251 caspase 3 Homo sapiens 210-219 34031270-13 2021 Our developed noninvasive apoptosis detection sensor (NIADS) indicated that imatinib induced cell apoptosis through caspase-3 activation. Imatinib Mesylate 76-84 caspase 3 Homo sapiens 116-125 33607534-9 2021 Moreover, combination of AZT/IMA suppressed cell viability, induced apoptosis and caspase3/7 activity more effectively and significantly compared to K562R cells treated with only IMA or AZT. Imatinib Mesylate 29-32 caspase 3 Homo sapiens 82-92 28612529-6 2017 CONCLUSION: The combination of IM and PP242 could increase the inhibition of PI3K/Akt/mTOR signaling pathway and apoptosis mediated by bax and caspase-3 in SUP-B15 cell line. Imatinib Mesylate 31-33 caspase 3 Homo sapiens 143-152 29298654-8 2018 Treatment of K562 cell lines with a combination of XT5 and imatinib-XT5 increased cytotoxicity, the Annexin V binding and caspase 3/7 activation. Imatinib Mesylate 59-67 caspase 3 Homo sapiens 122-131 26708080-7 2016 Results from the present study demonstrated that imatinib treatment inhibited cell viability, increased cell apoptosis, and significantly promoted caspase-3 and -9 activity in GCT. Imatinib Mesylate 49-57 caspase 3 Homo sapiens 147-163 28255316-6 2017 There was a significant up-regulation in caspase-3 enzyme activity and caspase-3 expression by imatinib and its half dose combination with DMC as compared to control. Imatinib Mesylate 95-103 caspase 3 Homo sapiens 41-50 28255316-6 2017 There was a significant up-regulation in caspase-3 enzyme activity and caspase-3 expression by imatinib and its half dose combination with DMC as compared to control. Imatinib Mesylate 95-103 caspase 3 Homo sapiens 71-80 25786656-9 2015 DU145 cells displayed diminished expression of anti-apoptotic Bcl-2 protein and augmented levels of caspase-8 and -9, as well as, increased enzymatic activity of caspase-3 in response to imatinib. Imatinib Mesylate 187-195 caspase 3 Homo sapiens 162-171 24930392-11 2015 Supranutritional dose of selenite when combined with imatinib induced apoptotic machinery by decreasing Bcl-2 expression, increasing caspase-3 activity and subsequently fragmenting DNA and blunted cytoprotective autophagy by decreasing Beclin-1 expression and autophagosomes formation. Imatinib Mesylate 53-61 caspase 3 Homo sapiens 133-142 24088895-9 2014 Sequential treatment with activin A and imatinib decreased Bcr-Abl, procaspase-3, Mcl-1, and Bcl-xL and also induced cleavage of procaspase-3/poly(ADP-ribose)polymerase. Imatinib Mesylate 40-48 caspase 3 Homo sapiens 68-80 25322553-5 2014 In addition, Gleevec activated caspase-3 and its downstream substrates PARP, and the caspase pan inhibitor Z-VAD-FMK (50 micromol x L(-1)) markedly reduced Gleevec-induced apoptosis from 47.97% +/- 10.56% to 31.05% +/- 9.206% (P < 0.05). Imatinib Mesylate 13-20 caspase 3 Homo sapiens 31-40 25322553-8 2014 In summary, Gleevec induced apoptosis in K562 cells via caspase-3 activation. Imatinib Mesylate 12-19 caspase 3 Homo sapiens 56-65 24527087-7 2014 Annexin V/propidium iodide and caspase-3 activity showed that imatinib induced apoptosis. Imatinib Mesylate 62-70 caspase 3 Homo sapiens 31-40 24088895-9 2014 Sequential treatment with activin A and imatinib decreased Bcr-Abl, procaspase-3, Mcl-1, and Bcl-xL and also induced cleavage of procaspase-3/poly(ADP-ribose)polymerase. Imatinib Mesylate 40-48 caspase 3 Homo sapiens 129-141 22388075-0 2012 Imatinib induces H2AX phosphorylation and apoptosis in chronic myelogenous leukemia cells in vitro via caspase-3/Mst1 pathway. Imatinib Mesylate 0-8 caspase 3 Homo sapiens 103-112 23434731-5 2013 Selective cleavage of T315I-mutant ABL mRNA by DNAzyme (T315I Dz) led to cell cycle arrest in G0/G1 phase, with induction of caspase-3/-7 in imatinib-resistant BCR-ABL-positive cells harboring the T315I mutation. Imatinib Mesylate 141-149 caspase 3 Homo sapiens 125-137 23613979-8 2013 Sequential treatment with ACM and imatinib induced Bcr-Abl down-regulation, cytochrome c release into the cytosol, and caspase-3 activation, as well as decreased Mcl-1 and Bcl-xL expressions, but did not affect Fas ligand/Fas death receptor and procaspase-8 expressions. Imatinib Mesylate 34-42 caspase 3 Homo sapiens 119-128 23613979-9 2013 ACM/imatinib sequential treatment-induced apoptosis was suppressed by a caspase-9 inhibitor and a caspase-3 inhibitor, indicating that the caspase cascade is involved in this apoptosis. Imatinib Mesylate 4-12 caspase 3 Homo sapiens 98-107 22388075-7 2012 Meanwhile, imatinib (1-8 mumol/L) activated caspase-3 and its downstream mammalian STE20-like kinase 1 (Mst1), and induced apoptosis of K562 cells. Imatinib Mesylate 11-19 caspase 3 Homo sapiens 44-53 22388075-8 2012 The caspase-3 inhibitor Z-VAD (40 mumol/L) reduced imatinib-induced H2AX phosphorylation at Ser139 and Tyr142 and blocked imatinib-induced apoptosis of K562 cells. Imatinib Mesylate 51-59 caspase 3 Homo sapiens 4-13 22388075-8 2012 The caspase-3 inhibitor Z-VAD (40 mumol/L) reduced imatinib-induced H2AX phosphorylation at Ser139 and Tyr142 and blocked imatinib-induced apoptosis of K562 cells. Imatinib Mesylate 122-130 caspase 3 Homo sapiens 4-13 22388075-10 2012 CONCLUSION: The caspase-3/Mst1 pathway is required for H2AX C-terminal phosphorylation at Ser139 and Tyr142 and subsequent apoptosis in Bcr-Abl-positive K562 cells induced by imatinib. Imatinib Mesylate 175-183 caspase 3 Homo sapiens 16-25 21658383-8 2011 Moreover, the apoptotic effect of imatinib (10 muM, 50 muM) after 24 h of exposure was demonstrated as evaluated by translocation of phosphatidylserine to external membrane leaflet and by increased activity of caspase-3. Imatinib Mesylate 34-42 caspase 3 Homo sapiens 210-219