PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32508033-0 2020 Tamoxifen induces fatty liver disease in breast cancer through the MAPK8/FoxO pathway. Tamoxifen 0-9 mitogen-activated protein kinase 8 Homo sapiens 67-72 33747968-9 2021 This pro-inflammatory M1-like skewing of TAMs in response to plinabulin was dependent on the JNK pathway. Tamoxifen 41-45 mitogen-activated protein kinase 8 Homo sapiens 93-96 32508033-4 2020 We found that mitogen-activated protein kinase 8 (MAPK8) was one DPT of TAM. Tamoxifen 72-75 mitogen-activated protein kinase 8 Homo sapiens 14-48 32508033-4 2020 We found that mitogen-activated protein kinase 8 (MAPK8) was one DPT of TAM. Tamoxifen 72-75 mitogen-activated protein kinase 8 Homo sapiens 50-55 32508033-10 2020 We verified that TAM may induce fatty liver in breast cancer through the MAPK8/FoxO signaling pathway. Tamoxifen 17-20 mitogen-activated protein kinase 8 Homo sapiens 73-78 21106355-7 2012 In addition, sp600125, the inhibitor of JNK, decreased the percentage of apoptosis induced by TAM in MCF-7 cells. Tamoxifen 94-97 mitogen-activated protein kinase 8 Homo sapiens 40-43 29386221-7 2018 Sensitization to tamoxifen is achieved via cAMP-mediated induction of unfolded protein response/ER stress pathway leading to activation of p38/JNK signaling and apoptosis. Tamoxifen 17-26 mitogen-activated protein kinase 8 Homo sapiens 143-146 29386221-9 2018 Finally, combining PDE4D inhibitors and tamoxifen suppressed tumor growth better than individual groups in vivoConclusions: PDE4D plays a pivotal role in acquired tamoxifen resistance via blocking cAMP/ER stress/p38-JNK signaling and apoptosis. Tamoxifen 40-49 mitogen-activated protein kinase 8 Homo sapiens 216-219 29386221-9 2018 Finally, combining PDE4D inhibitors and tamoxifen suppressed tumor growth better than individual groups in vivoConclusions: PDE4D plays a pivotal role in acquired tamoxifen resistance via blocking cAMP/ER stress/p38-JNK signaling and apoptosis. Tamoxifen 163-172 mitogen-activated protein kinase 8 Homo sapiens 216-219 28076660-5 2017 Tamoxifen-induced NS1ERT created a cytopathic phenotype and led to the activation of JNK and apoptosis. Tamoxifen 0-9 mitogen-activated protein kinase 8 Homo sapiens 85-88 26109525-4 2015 In the present study, tamoxifen was found to bring about autophagic cell death of human glioma cells that was accompanied by oxidative stress induction, JNK activation, downregulation of anti-autophagic BCL2 family members, viz. Tamoxifen 22-31 mitogen-activated protein kinase 8 Homo sapiens 153-156 26109525-6 2015 Oxidative stress induction appears to be primarily responsible for the tamoxifen-induced cell death since the cell death, JNK activation, and the alterations in the expression levels of BCL2 family members were abrogated on pretreatment with antioxidant vitamin E. Tamoxifen 71-80 mitogen-activated protein kinase 8 Homo sapiens 122-125 24658355-8 2014 These data suggest that tamoxifen-induced death of these cells is not dependent upon JNK signaling, but rather that ERK is the major MAPK driving their proliferation. Tamoxifen 24-33 mitogen-activated protein kinase 8 Homo sapiens 85-88 26329166-7 2015 In addition, we revealed that MKP1 inhibited tamoxifen-mediated JNK activation in tamoxifen resistant MCF7 and MCF7 cells, and by this mechanism MKP1 was able to inhibit tamoxifen-induced cell death. Tamoxifen 45-54 mitogen-activated protein kinase 8 Homo sapiens 64-67 26329166-7 2015 In addition, we revealed that MKP1 inhibited tamoxifen-mediated JNK activation in tamoxifen resistant MCF7 and MCF7 cells, and by this mechanism MKP1 was able to inhibit tamoxifen-induced cell death. Tamoxifen 82-91 mitogen-activated protein kinase 8 Homo sapiens 64-67 26329166-7 2015 In addition, we revealed that MKP1 inhibited tamoxifen-mediated JNK activation in tamoxifen resistant MCF7 and MCF7 cells, and by this mechanism MKP1 was able to inhibit tamoxifen-induced cell death. Tamoxifen 82-91 mitogen-activated protein kinase 8 Homo sapiens 64-67 26329166-9 2015 Collectively, our results indicated that MKP-1 can attenuate tamoxifen-induced cell death through inhibiting the JNK signal pathway, which represents a novel mechanism of tamoxifen resistance in MCF7 cells. Tamoxifen 61-70 mitogen-activated protein kinase 8 Homo sapiens 113-116 26329166-9 2015 Collectively, our results indicated that MKP-1 can attenuate tamoxifen-induced cell death through inhibiting the JNK signal pathway, which represents a novel mechanism of tamoxifen resistance in MCF7 cells. Tamoxifen 171-180 mitogen-activated protein kinase 8 Homo sapiens 113-116 18769129-4 2008 This data combined with previous reports that erbB2/Her2 and IGF-IR signals through JNK, led us to hypothesize that cytoplasmic accumulation of HuR may be a key contributor to development of tamoxifen resistance. Tamoxifen 191-200 mitogen-activated protein kinase 8 Homo sapiens 84-87 19935718-1 2010 The c-Jun N-terminal kinase (JNK) has been shown to mediate tamoxifen-induced apoptosis in breast cancer cells. Tamoxifen 60-69 mitogen-activated protein kinase 8 Homo sapiens 4-27 19935718-1 2010 The c-Jun N-terminal kinase (JNK) has been shown to mediate tamoxifen-induced apoptosis in breast cancer cells. Tamoxifen 60-69 mitogen-activated protein kinase 8 Homo sapiens 29-32 19935718-2 2010 However, the downstream mediators of the JNK pathway linking tamoxifen to effectors of apoptosis have yet to be identified. Tamoxifen 61-70 mitogen-activated protein kinase 8 Homo sapiens 41-44 19935718-3 2010 In this study, we analysed whether c-Jun, the major nuclear target of JNK, has a role in tamoxifen-induced apoptosis of SkBr3 breast cancer cells. Tamoxifen 89-98 mitogen-activated protein kinase 8 Homo sapiens 70-73 17307334-0 2007 Tamoxifen-induced activation of p21Waf1/Cip1 gene transcription is mediated by Early Growth Response-1 protein through the JNK and p38 MAP kinase/Elk-1 cascades in MDA-MB-361 breast carcinoma cells. Tamoxifen 0-9 mitogen-activated protein kinase 8 Homo sapiens 123-126 17307334-7 2007 In addition, induction of Egr-1 expression by TAM occurred at the transcriptional level via Ets-domain transcription factor Elk-1 through the JNK and p38 mitogen-activated protein (MAP) kinase pathways. Tamoxifen 46-49 mitogen-activated protein kinase 8 Homo sapiens 142-145 17307334-9 2007 We conclude that TAM stimulation of p21Waf1/Cip1 gene transcription in MDA-MB-361 cells depends largely on Elk-1-mediated Egr-1 expression induced by activation of the JNK and p38 MAP kinase pathways. Tamoxifen 17-20 mitogen-activated protein kinase 8 Homo sapiens 168-171 15606891-0 2005 Activated JNK brings about accelerated apoptosis of Bcl-2-overexpressing C6 glioma cells on treatment with tamoxifen. Tamoxifen 107-116 mitogen-activated protein kinase 8 Homo sapiens 10-13 16740736-8 2006 Furthermore, PD98059 increased the levels of phosphorylated c-Jun NH(2)-terminal kinase (JNK) in tamoxifen-treated MKP3-overexpressing cells, suggesting an interaction between MKP3 levels, activation of ERK1/2 MAPK, and JNK signaling in human breast cancer cells. Tamoxifen 97-106 mitogen-activated protein kinase 8 Homo sapiens 60-87 16740736-8 2006 Furthermore, PD98059 increased the levels of phosphorylated c-Jun NH(2)-terminal kinase (JNK) in tamoxifen-treated MKP3-overexpressing cells, suggesting an interaction between MKP3 levels, activation of ERK1/2 MAPK, and JNK signaling in human breast cancer cells. Tamoxifen 97-106 mitogen-activated protein kinase 8 Homo sapiens 89-92 16740736-8 2006 Furthermore, PD98059 increased the levels of phosphorylated c-Jun NH(2)-terminal kinase (JNK) in tamoxifen-treated MKP3-overexpressing cells, suggesting an interaction between MKP3 levels, activation of ERK1/2 MAPK, and JNK signaling in human breast cancer cells. Tamoxifen 97-106 mitogen-activated protein kinase 8 Homo sapiens 220-223 16450001-2 2006 We demonstrated here that long-term tamoxifen treatment causes G2/M cell cycle arrest through c-jun N-terminal kinase (JNK) activation, which is dependent on phosphorylation of Fas-associated death domain-containing protein (FADD) at 194 serine in an oestrogen (ER) receptor-positive breast cancer cell line, MCF-7. Tamoxifen 36-45 mitogen-activated protein kinase 8 Homo sapiens 94-117 16450001-2 2006 We demonstrated here that long-term tamoxifen treatment causes G2/M cell cycle arrest through c-jun N-terminal kinase (JNK) activation, which is dependent on phosphorylation of Fas-associated death domain-containing protein (FADD) at 194 serine in an oestrogen (ER) receptor-positive breast cancer cell line, MCF-7. Tamoxifen 36-45 mitogen-activated protein kinase 8 Homo sapiens 119-122 15606891-7 2005 Tamoxifen treatment of Bcl-2-overexpressing clones was found to result in activation of c-Jun N-terminal kinase (JNK) and p38 kinase. Tamoxifen 0-9 mitogen-activated protein kinase 8 Homo sapiens 88-111 15606891-7 2005 Tamoxifen treatment of Bcl-2-overexpressing clones was found to result in activation of c-Jun N-terminal kinase (JNK) and p38 kinase. Tamoxifen 0-9 mitogen-activated protein kinase 8 Homo sapiens 113-116 11106684-10 2000 However, AP-1-dependent transcription (P=.04) and phosphorylated c-Jun and JNK levels (P<.001) were statistically significantly increased in the tamoxifen-resistant tumors. Tamoxifen 148-157 mitogen-activated protein kinase 8 Homo sapiens 75-78 15388795-5 2005 We find that E2, as well as the antiestrogens tamoxifen (TAM) and ICI 182,780 (ICI), inhibit class II MHC expression through activation of the c-Jun N-terminal kinase (JNK) pathway. Tamoxifen 46-55 mitogen-activated protein kinase 8 Homo sapiens 143-166 15388795-5 2005 We find that E2, as well as the antiestrogens tamoxifen (TAM) and ICI 182,780 (ICI), inhibit class II MHC expression through activation of the c-Jun N-terminal kinase (JNK) pathway. Tamoxifen 46-55 mitogen-activated protein kinase 8 Homo sapiens 168-171 15388795-5 2005 We find that E2, as well as the antiestrogens tamoxifen (TAM) and ICI 182,780 (ICI), inhibit class II MHC expression through activation of the c-Jun N-terminal kinase (JNK) pathway. Tamoxifen 57-60 mitogen-activated protein kinase 8 Homo sapiens 143-166 15388795-5 2005 We find that E2, as well as the antiestrogens tamoxifen (TAM) and ICI 182,780 (ICI), inhibit class II MHC expression through activation of the c-Jun N-terminal kinase (JNK) pathway. Tamoxifen 57-60 mitogen-activated protein kinase 8 Homo sapiens 168-171 15388795-6 2005 Pharmacological JNK inhibitors reverse the inhibitory effects of E2, TAM, and ICI on class II MHC expression. Tamoxifen 69-72 mitogen-activated protein kinase 8 Homo sapiens 16-19 11145737-3 2001 Expression of constitutively active Src or stimulation of the endogenous Src/JNK pathway enhances transcriptional activation by the estrogen-ER complex and strongly stimulates the otherwise weak activation by the unliganded ER and the tamoxifen-ER complex. Tamoxifen 235-244 mitogen-activated protein kinase 8 Homo sapiens 77-80 14645110-5 2004 TAM induced the activation of ERK, c-Jun N-terminal protein kinase (JNK), and p38 with different time courses. Tamoxifen 0-3 mitogen-activated protein kinase 8 Homo sapiens 35-66 14645110-5 2004 TAM induced the activation of ERK, c-Jun N-terminal protein kinase (JNK), and p38 with different time courses. Tamoxifen 0-3 mitogen-activated protein kinase 8 Homo sapiens 68-71 14645110-7 2004 Either expression of dominant-negative JNK or pretreatment with SB203580 canceled the reduction of the number of viable cells by 5 microM TAM and inhibited the apoptotic nuclear changes and the cleavage of poly (ADP-ribose) polymerase induced by TAM. Tamoxifen 138-141 mitogen-activated protein kinase 8 Homo sapiens 39-42 11106684-11 2000 CONCLUSION: Our results suggest that the conversion of breast tumors to a tamoxifen-resistant phenotype is associated with oxidative stress and the subsequent antioxidant response and with increased phosphorylated JNK and c-Jun levels and AP-1 activity, which together could contribute to tumor growth. Tamoxifen 74-83 mitogen-activated protein kinase 8 Homo sapiens 214-217 11085519-7 2000 TAM also stimulated c-Jun NH2-terminal kinase (JNK) 1 activity, and interfering with the JNK pathway by over-expressing a DN JNK1 mutant attenuated TAM-induced apoptosis. Tamoxifen 0-3 mitogen-activated protein kinase 8 Homo sapiens 20-53 11085519-7 2000 TAM also stimulated c-Jun NH2-terminal kinase (JNK) 1 activity, and interfering with the JNK pathway by over-expressing a DN JNK1 mutant attenuated TAM-induced apoptosis. Tamoxifen 0-3 mitogen-activated protein kinase 8 Homo sapiens 47-50 11085519-7 2000 TAM also stimulated c-Jun NH2-terminal kinase (JNK) 1 activity, and interfering with the JNK pathway by over-expressing a DN JNK1 mutant attenuated TAM-induced apoptosis. Tamoxifen 0-3 mitogen-activated protein kinase 8 Homo sapiens 125-129 11085519-7 2000 TAM also stimulated c-Jun NH2-terminal kinase (JNK) 1 activity, and interfering with the JNK pathway by over-expressing a DN JNK1 mutant attenuated TAM-induced apoptosis. Tamoxifen 148-151 mitogen-activated protein kinase 8 Homo sapiens 125-129 11085519-8 2000 In addition, treatment of cells with a lipid-soluble antioxidant vitamin E blocked TAM-induced caspase-3 and JNK1 activation as well as apoptosis, whereas water-soluble antioxidants N-acetyl L-cysteine and glutathione had little effect. Tamoxifen 83-86 mitogen-activated protein kinase 8 Homo sapiens 109-113 11085519-9 2000 Thus, this study demonstrates that TAM induces apoptosis in ER-negative breast cancer cells through caspase-3 and JNK1 pathways, which are probably initiated at the cell membrane by an oxidative mechanism. Tamoxifen 35-38 mitogen-activated protein kinase 8 Homo sapiens 114-118 10037172-0 1999 Increased activator protein-1 DNA binding and c-Jun NH2-terminal kinase activity in human breast tumors with acquired tamoxifen resistance. Tamoxifen 118-127 mitogen-activated protein kinase 8 Homo sapiens 46-71 9090707-1 1997 PURPOSE: To study the signal transduction mechanisms of tamoxifen via the activation of MAPKs, JNK and ERK in order to understand its regulation of gene expression. Tamoxifen 56-65 mitogen-activated protein kinase 8 Homo sapiens 95-98 9090707-3 1997 RESULTS: TAM activated both JNK1 and ERK2 activities in a time- and dose-dependent manner in HeLa cells. Tamoxifen 9-12 mitogen-activated protein kinase 8 Homo sapiens 28-32 9090707-5 1997 CONCLUSIONS: These studies show that TAM activates the signal transduction kinases, JNK1 and ERK2, which may play important roles in the regulation of gene expression by TAM. Tamoxifen 37-40 mitogen-activated protein kinase 8 Homo sapiens 84-88 9090707-5 1997 CONCLUSIONS: These studies show that TAM activates the signal transduction kinases, JNK1 and ERK2, which may play important roles in the regulation of gene expression by TAM. Tamoxifen 170-173 mitogen-activated protein kinase 8 Homo sapiens 84-88