PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 31917290-10 2020 However, those above changes could be reversed by Compound C. In conclusion, this study indicated that DEX could reduce the inflammation and apoptosis of DOX-induced myocardial cells through activating the AMPK-GSK3beta signaling pathway. Doxorubicin 154-157 glycogen synthase kinase 3 beta Homo sapiens 211-219 25449432-7 2015 Furthermore, pantoprazole treatment resulted in a profound reduction of both total and phosphorylated forms of Akt and GSK-3beta, which in turn suppressed the adriamycin-induced Wnt/beta-catenin signaling in SGC7901/ADR cells. Doxorubicin 159-169 glycogen synthase kinase 3 beta Homo sapiens 119-128 30666159-0 2019 Peptidylarginine deiminase 4 overexpression resensitizes MCF-7/ADR breast cancer cells to adriamycin via GSK3beta/p53 activation. Doxorubicin 90-100 glycogen synthase kinase 3 beta Homo sapiens 105-113 32158616-5 2020 Glycogen synthase kinase 3beta (GSK3beta) promoted doxorubicin-mediated apoptosis, but this effect was abolished by overexpression of SIRT1 and AROS. Doxorubicin 51-62 glycogen synthase kinase 3 beta Homo sapiens 0-30 27523474-0 2016 MicroRNA-29a contributes to drug-resistance of breast cancer cells to adriamycin through PTEN/AKT/GSK3beta signaling pathway. Doxorubicin 70-80 glycogen synthase kinase 3 beta Homo sapiens 98-106 24407515-8 2014 However, resistance to doxorubicin and tamoxifen were alleviated in MCF-7/GSK-3beta(KD) cells upon co-treatment with an MEK inhibitor, indicating regulation of this resistance by the Raf/MEK/ERK pathway. Doxorubicin 23-34 glycogen synthase kinase 3 beta Homo sapiens 74-83 24407515-5 2014 MCF-7/GSK-3beta(KD) cells were more resistant to doxorubicin and tamoxifen compared with either MCF-7/GSK-3beta(WT) or MCF-7/GSK-3beta(A9) cells. Doxorubicin 49-60 glycogen synthase kinase 3 beta Homo sapiens 6-15 24407515-9 2014 Treatment of MCF-7 and MCF-7/GSK-3beta(WT) cells with doxorubicin eliminated the detection of S9-phosphorylated GSK-3beta, while total GSK-3beta was still detected. Doxorubicin 54-65 glycogen synthase kinase 3 beta Homo sapiens 29-38 24407515-6 2014 In the presence and absence of doxorubicin, the MCF-7/GSK-3beta(KD) cells formed more colonies in soft agar compared with MCF-7/GSK-3beta(WT) or MCF-7/GSK-3beta(A9) cells. Doxorubicin 31-42 glycogen synthase kinase 3 beta Homo sapiens 54-63 24407515-9 2014 Treatment of MCF-7 and MCF-7/GSK-3beta(WT) cells with doxorubicin eliminated the detection of S9-phosphorylated GSK-3beta, while total GSK-3beta was still detected. Doxorubicin 54-65 glycogen synthase kinase 3 beta Homo sapiens 112-121 24407515-9 2014 Treatment of MCF-7 and MCF-7/GSK-3beta(WT) cells with doxorubicin eliminated the detection of S9-phosphorylated GSK-3beta, while total GSK-3beta was still detected. Doxorubicin 54-65 glycogen synthase kinase 3 beta Homo sapiens 112-121 24407515-10 2014 In contrast, S9-phosphorylated GSK-3beta was still detected in MCF-7/GSK-3beta(KD) and MCF-7/GSK-3beta(A9) cells, indicating that one of the effects of doxorubicin on MCF-7 cells was suppression of S9-phosphorylated GSK-3beta, which could result in increased GSK-3beta activity. Doxorubicin 152-163 glycogen synthase kinase 3 beta Homo sapiens 31-40 24407515-11 2014 Taken together, these results demonstrate that introduction of GSK-3beta(KD) into MCF-7 breast cancer cells promotes resistance to doxorubicin and tamoxifen, but sensitizes the cells to mTORC1 blockade by rapamycin. Doxorubicin 131-142 glycogen synthase kinase 3 beta Homo sapiens 63-72 23248400-2 2012 This study sought to determine the usefulness of lithium chloride (LiCl) as a highly selective inhibitor of GSK-3beta to increase the sensitivity of LNCap cells to doxorubicin (Dox), etoposide (Eto), and vinblastine (Vin) drugs. Doxorubicin 164-175 glycogen synthase kinase 3 beta Homo sapiens 108-117 23248400-2 2012 This study sought to determine the usefulness of lithium chloride (LiCl) as a highly selective inhibitor of GSK-3beta to increase the sensitivity of LNCap cells to doxorubicin (Dox), etoposide (Eto), and vinblastine (Vin) drugs. Doxorubicin 177-180 glycogen synthase kinase 3 beta Homo sapiens 108-117 23408470-1 2012 Hormone-independent prostate cancer cell lines are resistant to antineoplastic drugs, this study sought to determine the usefulness of lithium chloride as an inhibitor of glycogen synthase kinase-3beta to increase the cytotoxic effect of doxorubicin, etoposide or vinblastine antineoplastic drugs on DU145 cells. Doxorubicin 238-249 glycogen synthase kinase 3 beta Homo sapiens 171-201 18701211-4 2008 Activation of GSK3beta induced translocation of survivin from the cytoplasm to the nucleus, resulting in G1 cell-cycle arrest and apoptosis, as well as sensitization to the chemotherapeutic drug doxorubicin. Doxorubicin 195-206 glycogen synthase kinase 3 beta Homo sapiens 14-22 17339365-9 2007 Increased Akt phosphorylation following treatment with doxorubicin was accompanied by increased phosphorylation of glycogen synthase kinase 3beta (GSK3beta) and FOXO3A, which are substrates of Akt (both GSK3beta and FOXO3A lose their proapoptotic activities when they are phosphorylated). Doxorubicin 55-66 glycogen synthase kinase 3 beta Homo sapiens 115-145 17339365-9 2007 Increased Akt phosphorylation following treatment with doxorubicin was accompanied by increased phosphorylation of glycogen synthase kinase 3beta (GSK3beta) and FOXO3A, which are substrates of Akt (both GSK3beta and FOXO3A lose their proapoptotic activities when they are phosphorylated). Doxorubicin 55-66 glycogen synthase kinase 3 beta Homo sapiens 147-155 17339365-9 2007 Increased Akt phosphorylation following treatment with doxorubicin was accompanied by increased phosphorylation of glycogen synthase kinase 3beta (GSK3beta) and FOXO3A, which are substrates of Akt (both GSK3beta and FOXO3A lose their proapoptotic activities when they are phosphorylated). Doxorubicin 55-66 glycogen synthase kinase 3 beta Homo sapiens 203-211 17339365-10 2007 Selenium reduced the abundance of phospho-GSK3beta induced by doxorubicin, whereas chemical inhibition of GSK3beta activity muted the apoptotic response to the selenium/doxorubicin combination. Doxorubicin 62-73 glycogen synthase kinase 3 beta Homo sapiens 42-50 17339365-10 2007 Selenium reduced the abundance of phospho-GSK3beta induced by doxorubicin, whereas chemical inhibition of GSK3beta activity muted the apoptotic response to the selenium/doxorubicin combination. Doxorubicin 169-180 glycogen synthase kinase 3 beta Homo sapiens 106-114