PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 15788689-10 2005 A JNK-independent suppression of survivin by SN38 and etoposide, but not by paclitaxel, was also observed. Etoposide 54-63 mitogen-activated protein kinase 8 Homo sapiens 2-5 15788689-7 2005 The JNK inhibitor SP600125 substantially decreased the activation of caspases and apoptosis induced by MSeA combination with SN38 or etoposide and completely blocked these events induced by MSeA/paclitaxel. Etoposide 133-142 mitogen-activated protein kinase 8 Homo sapiens 4-7 15001534-5 2004 It is noteworthy that pretreatment with paclitaxel significantly up-regulated MEKK1 expression, resulting in enhancement of etoposide- or cisplatin-induced MEKK1/MKK7-dependent JNK activation and apoptosis in LNCaP and DU145 cells. Etoposide 124-133 mitogen-activated protein kinase 8 Homo sapiens 177-180 10454518-3 1999 Induction of apoptotic cell death and DNA damage by treatment of U937 cells with etoposide (100 microM) was associated with phosphorylation and activation of the c-Jun NH(2)-terminal kinase (JNK1) SAPK enzymes p46 and p54-JNK2 and transient increases in expression of the transcription factor c-Jun, a primary JNK substrate. Etoposide 81-90 mitogen-activated protein kinase 8 Homo sapiens 191-195 12907245-0 2003 The JNK, ERK and p53 pathways play distinct roles in apoptosis mediated by the antitumor agents vinblastine, doxorubicin, and etoposide. Etoposide 126-135 mitogen-activated protein kinase 8 Homo sapiens 4-7 12707267-5 2003 We showed that JNK was activated by TRAIL and by etoposide and that the activation was enhanced by the combination of the two treatments. Etoposide 49-58 mitogen-activated protein kinase 8 Homo sapiens 15-18 12707267-8 2003 In cells treated with TRAIL plus etoposide, JNK inhibition increased cell survival and decreased apoptosis significantly. Etoposide 33-42 mitogen-activated protein kinase 8 Homo sapiens 44-47 12712406-8 2003 In addition, stable transfection with dominant-negative MKK7, by which JNK activation was inhibited, canceled both the up-regulation of Fas and the formation of DISC by etoposide. Etoposide 169-178 mitogen-activated protein kinase 8 Homo sapiens 71-74 12417047-3 2002 We found that the overexpression of FADD sensitizes etoposide-induced apoptosis through a rapid activation of c-Jun NH(2)-terminal kinase (JNK) and, subsequently, of caspase 3. Etoposide 52-61 mitogen-activated protein kinase 8 Homo sapiens 110-137 12417047-3 2002 We found that the overexpression of FADD sensitizes etoposide-induced apoptosis through a rapid activation of c-Jun NH(2)-terminal kinase (JNK) and, subsequently, of caspase 3. Etoposide 52-61 mitogen-activated protein kinase 8 Homo sapiens 139-142 12417047-7 2002 Interestingly, FADD was phosphorylated, and etoposide-induced JNK/caspase activation and apoptosis were enhanced in the cells arrested at G2/M transition, but not in those overexpressing mutant FADD, in which 194 serine was replaced by alanine. Etoposide 44-53 mitogen-activated protein kinase 8 Homo sapiens 62-65 12417047-8 2002 Our results demonstrate that phosphorylated FADD-dependent activation of the JNK/caspase pathway plays a pivotal role in sensitization to etoposide-induced apoptosis in prostate cancer cells. Etoposide 138-147 mitogen-activated protein kinase 8 Homo sapiens 77-80 10454518-3 1999 Induction of apoptotic cell death and DNA damage by treatment of U937 cells with etoposide (100 microM) was associated with phosphorylation and activation of the c-Jun NH(2)-terminal kinase (JNK1) SAPK enzymes p46 and p54-JNK2 and transient increases in expression of the transcription factor c-Jun, a primary JNK substrate. Etoposide 81-90 mitogen-activated protein kinase 8 Homo sapiens 191-194 12815281-8 2003 Based on the up-regulations observed at the mRNA level, it is speculated that etoposide-induced apoptosis in the HL-60 cells proceeds via pathways involving factors such as TNFalpha, IGFBP3, SAPK1, AP-1 and GADD153/CHOP10. Etoposide 78-87 mitogen-activated protein kinase 8 Homo sapiens 191-196 12663670-3 2003 We have observed that four DNA-damaging agents (cisplatin, actinomycin D, MMS, and etoposide), but not the cisplatin isomer, transplatin, which does not readily damage DNA, strongly activate JNK, p38, and extracellular signal-regulated kinase (ERK), and strongly increase phosphorylation and ATF2-dependent transcriptional activity. Etoposide 83-92 mitogen-activated protein kinase 8 Homo sapiens 191-194 12712406-0 2003 c-Jun NH2-terminal kinase-dependent Fas activation contributes to etoposide-induced apoptosis in p53-mutated prostate cancer cells. Etoposide 66-75 mitogen-activated protein kinase 8 Homo sapiens 0-25 8940082-4 1996 Treatment with vinblastine or etoposide (VP-16) also activated JNK, with maximum increases of 6.5- and 4.3-fold, respectively. Etoposide 30-39 mitogen-activated protein kinase 8 Homo sapiens 63-66 9533766-5 1998 2DG inhibited the etoposide-induced activation of c-Jun N-terminal kinase 1/stress-activated protein kinase (JNK1/SAPK) and the subsequent activation of CPP32, both of which are positive regulators for etoposide-induced apoptosis of U937 cells. Etoposide 18-27 mitogen-activated protein kinase 8 Homo sapiens 50-75 9533766-5 1998 2DG inhibited the etoposide-induced activation of c-Jun N-terminal kinase 1/stress-activated protein kinase (JNK1/SAPK) and the subsequent activation of CPP32, both of which are positive regulators for etoposide-induced apoptosis of U937 cells. Etoposide 18-27 mitogen-activated protein kinase 8 Homo sapiens 109-113 9533766-5 1998 2DG inhibited the etoposide-induced activation of c-Jun N-terminal kinase 1/stress-activated protein kinase (JNK1/SAPK) and the subsequent activation of CPP32, both of which are positive regulators for etoposide-induced apoptosis of U937 cells. Etoposide 202-211 mitogen-activated protein kinase 8 Homo sapiens 50-75 9020192-2 1997 In this study, we found that either etoposide (VP-16) or camptothecin (CPT) activated c-Jun N-terminal kinase 1/stress-activated protein kinase (JNK1/SAPK), transient c-jun expression, and ICE (interleukin-1beta converting enzyme)/CED-3-like proteases in U937 cells. Etoposide 36-45 mitogen-activated protein kinase 8 Homo sapiens 145-149 14646555-7 1997 Serum withdrawal-induced apoptosis was correlated with activation of JNK and suppression of ERK activities, while both JNK and ERK activities were slightly elevated during etoposid- induced apoptosis. Etoposide 172-180 mitogen-activated protein kinase 8 Homo sapiens 119-122 19424800-3 2009 Etoposide treatment or UV irradiation resulted in sustained activation of JNK, correlating with the induction of apoptosis. Etoposide 0-9 mitogen-activated protein kinase 8 Homo sapiens 74-77 30121250-9 2018 In summary, for the first time, we report that the stepwise JNK-AKT-NF-kappaB pathway is related to P-gp induction and DON elicited P-gp induction induces cells to resist exogenous toxic compounds, such as DON, Digoxin, Etoposide, etc. Etoposide 220-229 mitogen-activated protein kinase 8 Homo sapiens 60-63 22615609-11 2010 CONCLUSION: Taken together, our results indicate that etoposide induces cytotoxicity and WWOX phosphorylation and the cytotoxicty is augmented by blocking JNK pathway. Etoposide 54-63 mitogen-activated protein kinase 8 Homo sapiens 155-158 20552320-0 2009 Distinct roles for JNK1 and JNK3 during TNF-alpha- or etoposide-induced apoptosis in HeLa cells. Etoposide 54-63 mitogen-activated protein kinase 8 Homo sapiens 19-23 20552320-1 2009 Here, we show that JNK1 and JNK3 have different roles in TNF-alpha- or etoposide-induced apoptosis in HeLa cells. Etoposide 71-80 mitogen-activated protein kinase 8 Homo sapiens 19-23 22249269-9 2012 In addition, treatment with si-JNK greatly increased etoposide- and ionizing radiation (IR)-induced cell death in glioma spheres. Etoposide 53-62 mitogen-activated protein kinase 8 Homo sapiens 31-34 22615609-0 2010 Primary WWOX phosphorylation and JNK activation during etoposide induces cytotoxicity in HEK293 cells. Etoposide 55-64 mitogen-activated protein kinase 8 Homo sapiens 33-36 22615609-3 2010 Upon etoposide induced DNA damage, many stress signaling pathways including JNK are activated. Etoposide 5-14 mitogen-activated protein kinase 8 Homo sapiens 76-79 22615609-5 2010 In this study the activation of WWOX and JNK and their interaction following etoposide treatment were evaluated. Etoposide 77-86 mitogen-activated protein kinase 8 Homo sapiens 41-44 22615609-10 2010 Moreover, JNK inhibition enhances etoposide induced cytotoxicity in HEK293. Etoposide 34-43 mitogen-activated protein kinase 8 Homo sapiens 10-13 19424800-6 2009 Etoposide-induced JNK phosphorylation was unaffected by PKCdelta knockdown, implying that JNK can regulate apoptosis by PKCdelta-dependent and independent pathways, according to stimulus and cell type. Etoposide 0-9 mitogen-activated protein kinase 8 Homo sapiens 18-21 19424800-6 2009 Etoposide-induced JNK phosphorylation was unaffected by PKCdelta knockdown, implying that JNK can regulate apoptosis by PKCdelta-dependent and independent pathways, according to stimulus and cell type. Etoposide 0-9 mitogen-activated protein kinase 8 Homo sapiens 90-93 16709574-4 2006 Phosphorylation of Bax by JNK and p38 kinase activated after treatment with staurosporine, H(2)O(2), etoposide, and UV light was demonstrated by the shift in the pI value of Bax on two-dimensional gels and confirmed by metabolic labeling with inorganic [(32)P]phosphate in HepG2 cells. Etoposide 101-110 mitogen-activated protein kinase 8 Homo sapiens 26-29 19492242-0 2009 JWA sensitizes P-glycoprotein-mediated drug-resistant choriocarcinoma cells to etoposide via JNK and mitochondrial-associated signal pathway. Etoposide 79-88 mitogen-activated protein kinase 8 Homo sapiens 93-96 18164262-7 2008 However, a JNK-specific inhibitor, SP600125, strongly suppressed etoposide-induced eIF-4E phosphorylation. Etoposide 65-74 mitogen-activated protein kinase 8 Homo sapiens 11-14 18270325-10 2008 Taken together, we show that ceramide exhibits a mechanism of transcriptional regulation involving up-regulation of Txnip expression, also induced by etoposide, which results in ASK1 activation, ER stress, and p38 and JNK phosphorylation, all leading to apoptosis. Etoposide 150-159 mitogen-activated protein kinase 8 Homo sapiens 218-221 18174237-6 2008 Pretreatment of Sup-T1 cells with a specific JNK inhibitor, SP600125, also increased the Bim(EL) level and resensitized the cells to etoposide-induced apoptosis. Etoposide 133-142 mitogen-activated protein kinase 8 Homo sapiens 45-48 15832344-0 2005 JNK/p53 mediated cell death response in K562 exposed to etoposide-ionizing radiation combined treatment. Etoposide 56-65 mitogen-activated protein kinase 8 Homo sapiens 0-3 15832344-3 2005 In this study, we examined the role played by JNK/SAPK, p53, and mitochondrial pathways in cell death response of K562 cells to etoposide and IR treatment. Etoposide 128-137 mitogen-activated protein kinase 8 Homo sapiens 46-49 15832344-4 2005 Our results let us suppose that the induction of cell death, already evident in 15 Gy exposed cells, mainly in 15 Gy plus etoposide, may be mediated by JNK/SAPK pathway. Etoposide 122-131 mitogen-activated protein kinase 8 Homo sapiens 152-155 15832344-5 2005 Moreover, p53 is a potential substrate for JNK and may act as a JNK target for etoposide and ionizing radiation. Etoposide 79-88 mitogen-activated protein kinase 8 Homo sapiens 43-46 15832344-5 2005 Moreover, p53 is a potential substrate for JNK and may act as a JNK target for etoposide and ionizing radiation. Etoposide 79-88 mitogen-activated protein kinase 8 Homo sapiens 64-67