PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 31055231-11 2019 EA and its combination with DOX or DDP induced cell apoptosis through a pathway mediated by mitochondrial cytochrome c release. Cisplatin 35-38 cytochrome c, somatic Homo sapiens 106-118 32020220-8 2020 Mechanistically, Mdivi-1 upregulated Bax and downregulated Bcl-xL, leading to an increase in mitochondrial membrane permeability and subsequent release of cytochrome c from mitochondria into the cytosol, thereby aggravating cisplatin-induced apoptosis in HCC cells. Cisplatin 224-233 cytochrome c, somatic Homo sapiens 155-167 32047579-6 2020 Also, cisplatin-induced apoptosis in HL-60 cells was rescued through reservation of mitochondrial function, inhibition of cytochrome c release to cytosol, and suppression of caspase and PARP activation. Cisplatin 6-15 cytochrome c, somatic Homo sapiens 122-134 31897141-11 2020 Compared with cisplatin alone, co-treatment with beta-ELE increased cisplatin-mediated cytotoxicity against T24 cells, which resulted in the loss of mitochondrial membrane potential and release of cytochrome c into the cytoplasm. Cisplatin 68-77 cytochrome c, somatic Homo sapiens 197-209 31661694-0 2019 TRIAP1 Inhibition Activates the Cytochrome c/Apaf-1/Caspase-9 Signaling Pathway to Enhance Human Ovarian Cancer Sensitivity to Cisplatin. Cisplatin 127-136 cytochrome c, somatic Homo sapiens 32-44 30867764-9 2019 In addition, it was observed that celastrol/cisplatin upregulated the expression of Bcl-associated X protein, cytochrome c, caspase-3 and C/EBP homologous protein, and downregulated the expression of Bcl-2, poly(ADP-ribose) polymerase, 78 kDa glucose-regulated protein and caspase-9, whereas the expression of caspase-8 remained unchanged. Cisplatin 44-53 cytochrome c, somatic Homo sapiens 110-122 29523219-8 2018 In addition, cisplatin resulted in a more pronounced mitochondrial cytochrome c release into the cytoplasm in Hep-2 cells than in their resistant variants. Cisplatin 13-22 cytochrome c, somatic Homo sapiens 67-79 30563166-10 2018 Also, this combination treatment markedly increased the post-target cisplatin resistance pathway including bax, and cytochrome c expressions. Cisplatin 68-77 cytochrome c, somatic Homo sapiens 116-128 28214344-5 2017 Furthermore our results revealed that neferine combined with cisplatin down regulate the expression of Bcl-2 and up regulate the expression of Bax, Bad, Bak, release of cytochrome c, p53 levels, then activated cleavage forms of caspase-9, caspase-3, and PARP. Cisplatin 61-70 cytochrome c, somatic Homo sapiens 169-181 29467390-7 2018 Etoposide and cisplatin induced mitochondrial depolarization, cytochrome c release and caspase activation in COV434 cells. Cisplatin 14-23 cytochrome c, somatic Homo sapiens 62-74 29434943-7 2018 All compounds used alone (Pt12, cisplatin and the anti-MUC1 antibody) increased the concentration of proapoptotic Bax, cytochrome c and caspase-9 in comparison with control, thus suggesting that they activated the mitochondrial apoptotic pathway. Cisplatin 32-41 cytochrome c, somatic Homo sapiens 119-131 26403741-6 2015 The STOML-2-overexpressing cells exhibited an obvious resistance to IC50 Cisplatin-induced apoptosis as shown by both fluorescence microscopy and flow cytometry and presented with decreased expressions of cleaved caspase-3, Bax, and cytosol Cyt C and increased expressions of caspase-3, Bcl-2, and mitochondrial Cyt C. Cisplatin 73-82 cytochrome c, somatic Homo sapiens 241-246 27751820-8 2016 We show that PTMA silencing induces translocation of proapoptotic Bax to mitochondria and enhances cisplatin-induced cytochrome c release and caspase-9 activation. Cisplatin 99-108 cytochrome c, somatic Homo sapiens 117-129 26338199-6 2015 RT-PCR Array analysis showed that carbon ion beam combined with CDDP significantly induced apoptosis-related Cytochrome c, almost completely eliminated expression of the CSC markers CD44 and ESA, and significantly inhibited angiogenesis, and metastasis-related HIF1alpha and CD26 compared to carbon ion beam alone, X-ray alone, or X-ray combined with CDDP. Cisplatin 64-68 cytochrome c, somatic Homo sapiens 109-121 26925782-7 2016 Inhibition of PI3K/Aktactivity in A549/DDP cells and H460/DDP cells could reverse cisplatin resistance by enhancing the effect of cisplatin on Bax oligomerization and release of Cytochrome C, allowing activation of the caspase-mediated apoptosis pathway. Cisplatin 130-139 cytochrome c, somatic Homo sapiens 178-190 26403741-6 2015 The STOML-2-overexpressing cells exhibited an obvious resistance to IC50 Cisplatin-induced apoptosis as shown by both fluorescence microscopy and flow cytometry and presented with decreased expressions of cleaved caspase-3, Bax, and cytosol Cyt C and increased expressions of caspase-3, Bcl-2, and mitochondrial Cyt C. Cisplatin 73-82 cytochrome c, somatic Homo sapiens 312-317 26124336-4 2015 RESULTS: SFE sensitized cells to cisplatin by enhancing ROS and mitochondrial membrane depolarization that released cytochrome c and activated caspase 9 and caspase 3 in the mitochondrial pathway. Cisplatin 33-42 cytochrome c, somatic Homo sapiens 116-128 25567806-0 2015 The X-ray structure of the primary adducts formed in the reaction between cisplatin and cytochrome c. Cisplatin 74-83 cytochrome c, somatic Homo sapiens 88-100 25770930-5 2015 In addition, combination of chrysin and cisplatin promoted both extrinsic apoptosis by activating caspase-8 and intrinsic apoptosis by increasing the release of cytochrome c and activating caspase-9 in Hep G2 cells. Cisplatin 40-49 cytochrome c, somatic Homo sapiens 161-173 25894537-7 2015 In addition, decreased Bcl-2 expression and increased BID cleavage and cytochrome C release were detected in C2 cells after cisplatin challenge. Cisplatin 124-133 cytochrome c, somatic Homo sapiens 71-83 25796504-0 2015 Cisplatin-mediated c-myc overexpression and cytochrome c (cyt c) release result in the up-regulation of the death receptors DR4 and DR5 and the activation of caspase 3 and caspase 9, likely responsible for the TRAIL-sensitizing effect of cisplatin. Cisplatin 0-9 cytochrome c, somatic Homo sapiens 44-56 25796504-0 2015 Cisplatin-mediated c-myc overexpression and cytochrome c (cyt c) release result in the up-regulation of the death receptors DR4 and DR5 and the activation of caspase 3 and caspase 9, likely responsible for the TRAIL-sensitizing effect of cisplatin. Cisplatin 0-9 cytochrome c, somatic Homo sapiens 58-63 25796504-0 2015 Cisplatin-mediated c-myc overexpression and cytochrome c (cyt c) release result in the up-regulation of the death receptors DR4 and DR5 and the activation of caspase 3 and caspase 9, likely responsible for the TRAIL-sensitizing effect of cisplatin. Cisplatin 238-247 cytochrome c, somatic Homo sapiens 44-56 25796504-0 2015 Cisplatin-mediated c-myc overexpression and cytochrome c (cyt c) release result in the up-regulation of the death receptors DR4 and DR5 and the activation of caspase 3 and caspase 9, likely responsible for the TRAIL-sensitizing effect of cisplatin. Cisplatin 238-247 cytochrome c, somatic Homo sapiens 58-63 25796504-6 2015 Moreover, cisplatin increased the expression of c-myc in the presence of TRAIL, and there is a clear increase in cyt c release from mitochondria with the increasing concentrations of cisplatin. Cisplatin 183-192 cytochrome c, somatic Homo sapiens 113-118 25796504-8 2015 Together, we conclude that in TRAIL-treated MDR gastric carcinoma cells, cisplatin induces the death receptors DR4 and DR5 through the up-regulation of c-myc and strengthens the activation of caspases via promoting the release of cyt c. Cisplatin 73-82 cytochrome c, somatic Homo sapiens 230-235 25567806-1 2015 In the present study, the interactions between cisplatin and cytochrome c are investigated. Cisplatin 47-56 cytochrome c, somatic Homo sapiens 61-73 22397496-6 2012 Since this is a new cisplatin-resistant Calu1 cell line, it is noteworthy that DNA fragmentation, apoptotic cell ratio and cytochrome c levels were most decreased in the CR-Calu1 cell line. Cisplatin 20-29 cytochrome c, somatic Homo sapiens 123-135 22746312-5 2012 Multiple binding sites of cisplatin on cytochrome c were directly determined by FTICR MS combined with trypsin digestion without liquid chromatography (LC) separation. Cisplatin 26-35 cytochrome c, somatic Homo sapiens 39-51 22746312-6 2012 Four binding sites (Met65, Met80, His18, and His33) for cisplatin on cytochrome c were identified. Cisplatin 56-65 cytochrome c, somatic Homo sapiens 69-81 22746312-7 2012 Moreover, hydrogen/deuterium exchange (H/DX) combined with FTICR MS provides the sensitive method to insight the small conformation change of cytochrome c induced by cisplatin. Cisplatin 166-175 cytochrome c, somatic Homo sapiens 142-154 25216531-3 2014 Apollon knockdown increased cisplatin/docetaxel-induced apoptosis, mitochondrial dysfunction and cytochrome c release in two ESCC cell lines. Cisplatin 28-37 cytochrome c, somatic Homo sapiens 97-109 24627125-12 2014 The combination of beta-ELE and cisplatin enhanced the protein expression of cytochrome c, caspase-3 and Bad, and reduced protein levels of Bcl-2 and procaspase-3 in the A549/DDP lung cancer cells. Cisplatin 32-41 cytochrome c, somatic Homo sapiens 77-89 24563380-6 2014 The addition of Andro to CDDP induced synergistic apoptosis, which could be corroborated to the changes in protein and mRNA levels of Bax and Bcl-2, and the increased Fas/FasL association in these cells, resulting in increased release of cytochrome c, and activation of caspases. Cisplatin 25-29 cytochrome c, somatic Homo sapiens 238-250 24854102-2 2014 When compared with a blank control group, the proportion of apoptotic cells undergoing Beclin 1 interfering increased significantly after cisplatin treatment, accompanied by reduction in mitochondrial membrane potential, increase in activities of caspase-9/3 and cytoplasmic cytochrome C, elevation of Bax expression, and reduction in Bcl-2 expression. Cisplatin 138-147 cytochrome c, somatic Homo sapiens 275-287 22971517-4 2013 In cells treated with cisplatin, 30muM alpha-TOS prominently attenuated the manifestation of characteristic features of apoptosis - release of cytochrome c from mitochondria, caspase-3-like activity, and cleavage of poly(ADP-ribose) polymerase. Cisplatin 22-31 cytochrome c, somatic Homo sapiens 143-155 23720056-7 2013 Immunofluorescent analyses showed clear overlap between TR3 and mitochondrial Hsp60 in cisplatin-treated cells, which was associated with cytochrome c release. Cisplatin 87-96 cytochrome c, somatic Homo sapiens 138-150 23665025-8 2013 We found that the combination of cisplatin and STAT3 siRNA resulted in the collapse of the mitochondrial membrane potential, attenuated the expression of Bcl-xL and Bcl-2, and increased the release of cytochrome C and expression of Bax. Cisplatin 33-42 cytochrome c, somatic Homo sapiens 201-213 23277286-6 2013 Furthermore, beta-elemene plus cisplatin exposure significantly disrupted the mitochondrial transmembrane potential (DeltaPsi (m)) and increased the release of cytochrome c from mitochondria into the cytoplasm. Cisplatin 31-40 cytochrome c, somatic Homo sapiens 176-188 22281241-2 2012 Here we show that cisplatin induces mitochondrial proteins such as Smac/DIABLO, Cytochrome c, and HrtA2/Omi release to the cytosol and apoptosis in cisplatin-sensitive, but not -resistant ovarian cancer cells. Cisplatin 18-27 cytochrome c, somatic Homo sapiens 80-92 22746312-0 2012 Probing the interaction of cisplatin with cytochrome C by electrospray ionization Fourier transform ion cyclotron resonance mass spectrometry. Cisplatin 27-36 cytochrome c, somatic Homo sapiens 42-54 22746312-2 2012 Here, the interaction of cisplatin with cytochrome c was investigated using Fourier transform ion cyclotron resonance mass spectrometry (FTICR MS). Cisplatin 25-34 cytochrome c, somatic Homo sapiens 40-52 21798574-8 2012 In the in vitro experiments with cell lines, silencing of optic atrophy 1 expression reduced cisplatin resistance, which was further shown via increased release of cytochrome c and activation of caspase-dependent apoptotic pathway. Cisplatin 93-102 cytochrome c, somatic Homo sapiens 164-176 21676925-9 2011 In ESCC cells treated with cisplatin, a common chemotherapeutic drug, Smac and cytochrome c were released from mitochondria, and caspase-3 and caspase-9 were activated. Cisplatin 27-36 cytochrome c, somatic Homo sapiens 79-91 21676925-10 2011 Knockdown of Smac abrogated cisplatin-induced apoptosis, mitochondrial dysfunction, cytochrome c release, and caspase activation. Cisplatin 28-37 cytochrome c, somatic Homo sapiens 84-96 17363497-4 2007 A comparative analysis of molecular events underlying cell death in bortezomib-treated versus cisplatin-treated H460 cells revealed that bortezomib, but not cisplatin, caused a rapid and abundant release of cytochrome c and Smac/DIABLO from mitochondria. Cisplatin 94-103 cytochrome c, somatic Homo sapiens 207-219 21160028-10 2011 These MEFs were more sensitive to cisplatin-induced Bax activation, release of cytochrome c, and apoptosis. Cisplatin 34-43 cytochrome c, somatic Homo sapiens 79-91 20654585-8 2010 Although, cisplatin-induced apoptosis was associated with the translocation of Bax to mitochondria, release of cytochrome c and caspase-3/7 activation, the levels of relocalized Bax and cytochrome c were significantly greater following GSTP1 knockdown. Cisplatin 10-19 cytochrome c, somatic Homo sapiens 111-123 20654585-8 2010 Although, cisplatin-induced apoptosis was associated with the translocation of Bax to mitochondria, release of cytochrome c and caspase-3/7 activation, the levels of relocalized Bax and cytochrome c were significantly greater following GSTP1 knockdown. Cisplatin 10-19 cytochrome c, somatic Homo sapiens 186-198 19258036-4 2009 Cisplatin-stimulated plaa(high) cells contained significantly higher levels of DNA fragmentation, caspase 3, 8 and 9 activities, PLA(2) enzyme activity, and cytochrome c leakage from mitochondria than did the cisplatin-stimulated plaa(low) cells. Cisplatin 0-9 cytochrome c, somatic Homo sapiens 157-169 19258036-6 2009 Cisplatin-induced-cytochrome c leakage in plaa(high) cells was reduced by siRNA-PLAA and restored by the addition of exogenous arachidonic acid (AA), suggesting to us that PLAA induction by cisplatin promoted cytochrome c leakage/mitochondrial damage partially by accumulating AA. Cisplatin 0-9 cytochrome c, somatic Homo sapiens 18-30 19258036-6 2009 Cisplatin-induced-cytochrome c leakage in plaa(high) cells was reduced by siRNA-PLAA and restored by the addition of exogenous arachidonic acid (AA), suggesting to us that PLAA induction by cisplatin promoted cytochrome c leakage/mitochondrial damage partially by accumulating AA. Cisplatin 0-9 cytochrome c, somatic Homo sapiens 209-221 19258036-6 2009 Cisplatin-induced-cytochrome c leakage in plaa(high) cells was reduced by siRNA-PLAA and restored by the addition of exogenous arachidonic acid (AA), suggesting to us that PLAA induction by cisplatin promoted cytochrome c leakage/mitochondrial damage partially by accumulating AA. Cisplatin 190-199 cytochrome c, somatic Homo sapiens 18-30 19276256-10 2009 Furthermore, the combination of lexatumumab and cisplatin significantly enhanced caspase-8 activity, Bid cleavage, up-regulation of Bax, cytochrome c release, and caspase-9, caspase-6, and caspase-3 activities. Cisplatin 48-57 cytochrome c, somatic Homo sapiens 137-149 17619073-7 2007 Similar to function way of SM, cDDP causes cancer cell apoptosis though caspase-8/caspase-3 and Bax/cytochrome c pathways, but the resistance to cDDP is correlated with Bcl-2 and Bcl-xL overexpression. Cisplatin 31-35 cytochrome c, somatic Homo sapiens 100-112 17619073-9 2007 The combined treatment of SM and cDDP significantly reduced Bcl-2 and Bcl-xL expressions, and enhanced Bax, cytochrome c, caspase-9 and -3 expressions in breast cancer cells. Cisplatin 33-37 cytochrome c, somatic Homo sapiens 108-120 17311906-6 2007 Cisplatin-induced loss of Mcl-1 occurs at the same time as the mitochondrial release of cytochrome c, activation of caspase-3, and initiation of apoptosis. Cisplatin 0-9 cytochrome c, somatic Homo sapiens 88-100 22545969-7 2010 beta-Elemene augmented the cisplatin-induced activation of caspase-3/7/10 and caspase-9, cleavage of caspase-3 and -9, suppression of Bcl-2 and Bcl-X(L) expression, and release of cytochrome c from mitochondria in these cells. Cisplatin 27-36 cytochrome c, somatic Homo sapiens 181-193 19889954-6 2010 During cisplatin treatment, Bax translocated to mitochondria, leading to cytochrome c release. Cisplatin 7-16 cytochrome c, somatic Homo sapiens 73-85 19286393-0 2009 Direct determination of the primary binding site of cisplatin on cytochrome C by mass spectrometry. Cisplatin 52-61 cytochrome c, somatic Homo sapiens 65-77 19286393-3 2009 The monoadduct cytochrome c-Pt(NH(3))(2)(H(2)O) is found to be the primary adduct produced by the cytochrome c-cisplatin interactions under native conditions. Cisplatin 111-120 cytochrome c, somatic Homo sapiens 15-27 19286393-3 2009 The monoadduct cytochrome c-Pt(NH(3))(2)(H(2)O) is found to be the primary adduct produced by the cytochrome c-cisplatin interactions under native conditions. Cisplatin 111-120 cytochrome c, somatic Homo sapiens 98-110 19286393-4 2009 To locate the primary binding site of cisplatin, both free cytochrome c and the cytochrome c adducts underwent trypsin digestion, followed by Fourier transform mass spectrometry (FT-MS) to identify unique fragments in the adduct digest. Cisplatin 38-47 cytochrome c, somatic Homo sapiens 59-71 19286393-4 2009 To locate the primary binding site of cisplatin, both free cytochrome c and the cytochrome c adducts underwent trypsin digestion, followed by Fourier transform mass spectrometry (FT-MS) to identify unique fragments in the adduct digest. Cisplatin 38-47 cytochrome c, somatic Homo sapiens 80-92 19286393-7 2009 The product-ion spectra of the four fragments reveal that Met65 is the primary binding site of cisplatin on cytochrome c. Cisplatin 95-104 cytochrome c, somatic Homo sapiens 108-120 19286655-4 2009 In this report, we demonstrate MMR protein-dependent relocalization of cytochrome c to the cytoplasm and cleavage of caspase-9, caspase-3, and poly(ADP-ribose) polymerase upon treatment of cells with CDDP. Cisplatin 200-204 cytochrome c, somatic Homo sapiens 71-83 19351772-9 2009 Bid protein processing in truncated t-Bid and cytochrome c release from mitochondria are significantly increased in the presence of valproate, providing a mechanistic rationale for improvement of the proapoptotic efficacy of cisplatin and pemetrexed. Cisplatin 225-234 cytochrome c, somatic Homo sapiens 46-58 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. Cisplatin 0-4 cytochrome c, somatic Homo sapiens 146-158 18214855-4 2008 After cisplatin treatment, calpain was activated, resulting in Bid cleavage at 4-5 hr, followed by Bid translocation and cytochrome c release, leading to cell death. Cisplatin 6-15 cytochrome c, somatic Homo sapiens 121-133 18214855-9 2008 The delays of cytochrome c release, caspase-3 activation and subsequent cell death by inactivating calpain or silencing Bid exclude other earlier or parallel pathways, strongly suggesting that the calpain-mediated pathway is the kinetically earliest one, which dominates the cisplatin-induced apoptosis. Cisplatin 275-284 cytochrome c, somatic Homo sapiens 14-26 18451495-4 2008 Combined treatment with berberine and cisplatin acted in concert to induce loss of mitochondrial membrane potential (Delta Psi m), release of cytochrome-c from mitochondria, and decreased expression of antiapoptotic Bcl-2, Bcl-x/L, resulting in activation of caspases and apoptosis. Cisplatin 38-47 cytochrome c, somatic Homo sapiens 142-154 17603269-11 2007 TP inhibited activation of caspase 3, 9 and mitochondrial cytochrome c release induced by cisplatin. Cisplatin 90-99 cytochrome c, somatic Homo sapiens 58-70 17311906-11 2007 The proteasome inhibitors effectively blocked cisplatin-induced mitochondrial release of cytochrome c, caspase-3 activation, and apoptosis. Cisplatin 46-55 cytochrome c, somatic Homo sapiens 89-101 16442262-9 2006 In addition, cisplatin-induced apoptosis is abrogated by the overexpression of either Bcl-2 or Bcl-x(L), which diminished changes of mitochondrial membrane potential and decreased the amount of cytochrome c released from mitochondria. Cisplatin 13-22 cytochrome c, somatic Homo sapiens 194-206 16855374-4 2006 RESULTS: Exposure to cDDP, induced apoptosis via the mitochondrial apoptotic pathway as evidenced by cytochrome c release and caspase activation. Cisplatin 21-25 cytochrome c, somatic Homo sapiens 101-113 16228292-5 2005 Cisplatin exerted same effects on cell viability and apoptosis in both cells, but released smaller amounts of cytochrome c while activated more caspase-8 in MCF-7/E6. Cisplatin 0-9 cytochrome c, somatic Homo sapiens 110-122 16540663-5 2006 Here we show that CDDP induces mitochondrial p53 accumulation, the mitochondrial release of Smac, cytochrome c, and HTR/Omi, and apoptosis in chemosensitive but not in resistant ovarian cancer cells. Cisplatin 18-22 cytochrome c, somatic Homo sapiens 98-110 16009487-6 2006 Western blot analysis of subcellular fractions showed that cisplatin induced redistribution of Bax and cytochrome c. Cisplatin 59-68 cytochrome c, somatic Homo sapiens 103-115 12618201-6 2003 However, two apoptosome molecules, cytochrome c and Apaf-1, were significantly augmented in the cytoplasm by CDDP treatment. Cisplatin 109-113 cytochrome c, somatic Homo sapiens 35-47 15870947-4 2005 Cisplatin treatment induced the activation of caspase-8, -9 and -3 and the release of cytochrome c in apoptosis-sensitive Ma-46. Cisplatin 0-9 cytochrome c, somatic Homo sapiens 86-98 15965098-5 2005 The release of mitochondrial cytochrome c into cytosol by cisplatin was enhanced more obviously in 143B cells than in 143B-rho0 cells; however, in the control group of 143B-rho0 cells, it was already dramatically greater. Cisplatin 58-67 cytochrome c, somatic Homo sapiens 29-41 15965098-6 2005 Depletion of mtDNA may increase sensitivity of cells to cisplatin-induced apoptosis by enhancing caspase 3 activation via both cytochrome c-dependent and -independent pathways. Cisplatin 56-65 cytochrome c, somatic Homo sapiens 127-139 15604295-7 2004 CDDP treatment induced the activation and redistribution of cytosolic Bax and the release of cytochrome c from injured mitochondria. Cisplatin 0-4 cytochrome c, somatic Homo sapiens 93-105 15153331-8 2004 Indeed, GSH ethyl ester-mediated increase of GSH abrogated apoptosis induced by cisplatin and melphalan by inhibition of Bax/cytochrome c redistribution. Cisplatin 80-89 cytochrome c, somatic Homo sapiens 125-137 12867996-6 2003 On the other hand, while all apoptosis-inducing treatments and treatment with 2 mM H(2)O(2) caused Bax translocation from the cytosol to mitochondria as well as cytochrome c release from mitochondria to the cytosol, treatment with BSO plus cisplatin did not. Cisplatin 240-249 cytochrome c, somatic Homo sapiens 161-173 12893210-0 2003 Enhancement of sensitivity to cisplatin by orobol is associated with increased mitochondrial cytochrome c release in human ovarian carcinoma cells. Cisplatin 30-39 cytochrome c, somatic Homo sapiens 93-105 12667321-0 2002 [Relationship between cytochrome c-mediated caspase-3 activity and chemoresistance in cisplatin-resistant human ovarian cancer cell lines]. Cisplatin 86-95 cytochrome c, somatic Homo sapiens 22-34 12543167-9 2003 On the other hand, following cisplatin treatment, the same degree of increase in cytoplasmic Cyt c was detected in both HSC-2 and HSC-2CR. Cisplatin 29-38 cytochrome c, somatic Homo sapiens 93-98 12667321-1 2002 OBJECTIVE: To investigate the effects of anti-apoptosis gene (bcl-X(L)), cytochrome c and caspase-3 activity on chemoresistance in cisplatin-resistant human ovarian cancer cell lines (A2780/DDP, COC1/DDP). Cisplatin 131-140 cytochrome c, somatic Homo sapiens 73-85 12667321-2 2002 METHODS: The expression of bcl-X(L) cisplatin treated cytochrome c and caspase-3 activity were monitored by RT-PCR and Western blot in cisplatin-resistant (A2780/DDP, COC1/DDP) and cisplatin-sensitive (A2780, COC1) cell lines. Cisplatin 36-45 cytochrome c, somatic Homo sapiens 54-66 12667321-2 2002 METHODS: The expression of bcl-X(L) cisplatin treated cytochrome c and caspase-3 activity were monitored by RT-PCR and Western blot in cisplatin-resistant (A2780/DDP, COC1/DDP) and cisplatin-sensitive (A2780, COC1) cell lines. Cisplatin 135-144 cytochrome c, somatic Homo sapiens 54-66 12667321-2 2002 METHODS: The expression of bcl-X(L) cisplatin treated cytochrome c and caspase-3 activity were monitored by RT-PCR and Western blot in cisplatin-resistant (A2780/DDP, COC1/DDP) and cisplatin-sensitive (A2780, COC1) cell lines. Cisplatin 135-144 cytochrome c, somatic Homo sapiens 54-66 12667321-5 2002 CONCLUSION: The overexpression of anti-apoptotic gene bcl-X(L), which downregulates cytochrome c and decreases caspase-3 activity, may be related to cisplatin-resistance in human ovarian cancer cell lines. Cisplatin 149-158 cytochrome c, somatic Homo sapiens 84-96 12060385-4 2002 Etoposide and cisplatin induced apoptosis in drug-sensitive MeWo cells as indicated by dose-dependent (i) cytochrome c release, (ii) caspase activation, (iii) DNA fragmentation, and (iv) cleavage of poly(ADP-ribose)polymerase. Cisplatin 14-23 cytochrome c, somatic Homo sapiens 106-118 12060385-6 2002 Highly cisplatin-resistant cells (MeWo(Cis1)), however, demonstrated a reduced caspase 9 activity and cytochrome c release but the extent of effector caspase activation as well as DNA fragmentation was comparable to that of sensitive MeWo cells at equitoxic concentrations. Cisplatin 7-16 cytochrome c, somatic Homo sapiens 102-114 11895917-7 2002 Furthermore, cisplatin alone was unable to induce the mitochondrial apoptotic events; however, the rituximab-cisplatin combination was able to synergistically induce significant apoptosis and mitochondria-mediated apoptotic events [mitochondrial membrane depolarization (DeltaPsi(m)), cytochrome c release from mitochondria, and caspase-3 and -9 activation]. Cisplatin 109-118 cytochrome c, somatic Homo sapiens 285-297 12018840-5 2002 Cisplatin induced apoptosis with the cytochrome c release and caspase-3 activation in both wild-type and caspase-8-deficient JB-6 cells, while the Fas antibody induced these apoptotic events only in wild-type cells. Cisplatin 0-9 cytochrome c, somatic Homo sapiens 37-49 12018840-10 2002 These data suggest that the cisplatin-induced apoptotic signal is initiated by the caspase-8-independent cytochrome c release, and the JNK activation protects cells from cisplatin-induced apoptosis via the metallothionein expression. Cisplatin 28-37 cytochrome c, somatic Homo sapiens 105-117 11895373-0 2002 Cisplatin-induced apoptosis of DRG neurons involves bax redistribution and cytochrome c release but not fas receptor signaling. Cisplatin 0-9 cytochrome c, somatic Homo sapiens 75-87 11895373-5 2002 However, cisplatin treatment of DRG caused redistribution of cytosolic bax and mitochondrial release of cytochrome c. Cisplatin 9-18 cytochrome c, somatic Homo sapiens 104-116 11905052-6 2002 Because caspase-9 activation requires the release of mitochondorial cytochrome c (Cyt c) into the cytoplasm, we determined the level of cytoplasmic Cyt c in response to cisplatin treatment. Cisplatin 169-178 cytochrome c, somatic Homo sapiens 68-80 11905052-6 2002 Because caspase-9 activation requires the release of mitochondorial cytochrome c (Cyt c) into the cytoplasm, we determined the level of cytoplasmic Cyt c in response to cisplatin treatment. Cisplatin 169-178 cytochrome c, somatic Homo sapiens 82-87 11905052-6 2002 Because caspase-9 activation requires the release of mitochondorial cytochrome c (Cyt c) into the cytoplasm, we determined the level of cytoplasmic Cyt c in response to cisplatin treatment. Cisplatin 169-178 cytochrome c, somatic Homo sapiens 148-153 11905052-7 2002 Interestingly, following cisplatin treatment, the same extent of increase in cytoplasmic Cyt c was evident and the expression of Bcl-2 family proteins (Bcl-2 and Bcl-XL) remained unchanged in both CRHNSCCs and CSHNSCCs. Cisplatin 25-34 cytochrome c, somatic Homo sapiens 89-94 11566177-8 2001 The accumulation of cytosolic cytochrome c, an activator of caspase-9, and the induction of the mitochondrial membrane-associated voltage-dependent anion channel were also reduced in cisplatin-resistant cells. Cisplatin 183-192 cytochrome c, somatic Homo sapiens 30-42 11774739-6 2001 Cytochrome C (CytC) in MT was released from MT into cytoplasm in response to cisplatin treatment in Pt-sensitive cells, whereas up-regulation of CytC level in MT rather than CytC release from MT was observed in Pt-resistant cells. Cisplatin 77-86 cytochrome c, somatic Homo sapiens 0-12 11774739-6 2001 Cytochrome C (CytC) in MT was released from MT into cytoplasm in response to cisplatin treatment in Pt-sensitive cells, whereas up-regulation of CytC level in MT rather than CytC release from MT was observed in Pt-resistant cells. Cisplatin 77-86 cytochrome c, somatic Homo sapiens 14-18 10993883-5 2000 Cisplatin-induced apoptosis was associated with cytochrome c release and subsequent caspase-3 activation, both of which could be prevented by treatment with the MEK inhibitors. Cisplatin 0-9 cytochrome c, somatic Homo sapiens 48-60 11340162-5 2001 We report that expression of a kinase-inactive fragment of MEKK1 (dominant negative MEKK [dnMEKK]) efficiently blocked cisplatin-induced modulation of Bak and cytochrome c release and consequently also reduced DEVDase activation and nuclear fragmentation. Cisplatin 119-128 cytochrome c, somatic Homo sapiens 159-171 11368186-2 2001 The present study revealed that administration of cis-diamminedichloroplatinum(II)-elicited oxidative stress in renal mitochondria, decreased the renal expression of Bcl-x, released cytochrome c from mitochondria to cytosol, and induced apoptosis and renal dysfunction by a mechanism that was inhibited by AH-SOD. Cisplatin 50-82 cytochrome c, somatic Homo sapiens 182-194 9014341-0 1997 Studies on the interaction between cytochrome c and cis-PtCl2(NH3)2. Cisplatin 52-67 cytochrome c, somatic Homo sapiens 35-47 10918609-3 2000 Etoposide, cisplatin and tumor necrosis factor-alpha induced apoptosis of C6 rat glioma cells which was associated with ceramide formation due to activation of neutral sphingomyelinase, followed by release of mitochondrial cytochrome c into the cytosol and activation of caspases-9 and -3. Cisplatin 11-20 cytochrome c, somatic Homo sapiens 223-235 10397248-5 1999 Because the activation of procaspase-3 by caspase-9 requires the release of cytochrome c into the cytoplasm, we determined the level of cytoplasmic cytochrome c in each cell line in response to cisplatin treatment. Cisplatin 194-203 cytochrome c, somatic Homo sapiens 148-160 10397248-6 1999 Consistent with the caspase-3 activation data, a very small increase in cytoplasmic cytochrome c was observed in A2780 cells following cisplatin treatment, whereas dramatic increases were evident in both the CP70 and C30 cell lines. Cisplatin 135-144 cytochrome c, somatic Homo sapiens 84-96 10969782-2 2000 We present evidence that apoptosis of caspase-3-deficient MCF-7 breast cancer cells is defective in response to cisplatin treatment, as determined by chromatin condensation, nuclear fragmentation, DNA fragmentation, and release of cytochrome c from the mitochondria. Cisplatin 112-121 cytochrome c, somatic Homo sapiens 231-243 9014341-1 1997 The interactions between cytochrome c and cis-PtCl2(NH3)2 under different conditions are reported. Cisplatin 42-57 cytochrome c, somatic Homo sapiens 25-37 9014341-2 1997 It is found that cis-PtCl2(NH3)2 is highly selective to bind to sulfur-containing Met residue and the interaction mode of cis-PtCl2(NH3)2 with cytochrome c is different from that of PtCl4(2-) with cytochrome c. Cisplatin 17-32 cytochrome c, somatic Homo sapiens 143-155 9014341-2 1997 It is found that cis-PtCl2(NH3)2 is highly selective to bind to sulfur-containing Met residue and the interaction mode of cis-PtCl2(NH3)2 with cytochrome c is different from that of PtCl4(2-) with cytochrome c. Cisplatin 17-32 cytochrome c, somatic Homo sapiens 197-209 9014341-2 1997 It is found that cis-PtCl2(NH3)2 is highly selective to bind to sulfur-containing Met residue and the interaction mode of cis-PtCl2(NH3)2 with cytochrome c is different from that of PtCl4(2-) with cytochrome c. Cisplatin 122-137 cytochrome c, somatic Homo sapiens 143-155 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. Cisplatin 196-205 cytochrome c, somatic Homo sapiens 105-117 33929634-5 2021 Our results found that 25 ng/ml resistin could significantly increase cisplatin-induced apoptosis and G2/M phase arrest, enhance reactive oxygen species generation, exacerbate the collapse of mitochondrial membrane potential, promote the distribution of cytochrome C in the cytoplasm from mitochondria, and activate caspase 3. Cisplatin 70-79 cytochrome c, somatic Homo sapiens 254-266 32881246-7 2020 However, PIO decreased the generation of ROS, opening of mPTP, dissipation of MMP and translocation of cytochrome c after cisplatin treatment. Cisplatin 122-131 cytochrome c, somatic Homo sapiens 103-115 35204233-8 2022 In addition, the depletion of LPA3 enhances cisplatin-induced cytochrome C releasing. Cisplatin 44-53 cytochrome c, somatic Homo sapiens 62-74 33202209-5 2020 Indeed, cytochrome c release in the cells with BNIP3 knockout and knockdown was higher than in the wild-type (WT) upon apoptosis stimulation by cisplatin. Cisplatin 144-153 cytochrome c, somatic Homo sapiens 8-20