PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26041409-0 2015 Src/STAT3-dependent heme oxygenase-1 induction mediates chemoresistance of breast cancer cells to doxorubicin by promoting autophagy. Doxorubicin 98-109 heme oxygenase 1 Homo sapiens 20-36 31319070-11 2019 In summary, nicorandil may protect HUVECs from DOX-induced apoptosis, in part through ATF3-mediated Nrf2/HO-1 signaling pathways, which potentially protect the vessels from severe DOX toxicity. Doxorubicin 47-50 heme oxygenase 1 Homo sapiens 105-109 30159756-1 2018 Doxorubicin (Dox)-induced cardiotoxicity, a limiting factor in the use of Dox to treat cancer, can be mitigated by the mitogenic factor FGF2 in vitro, via a heme oxygenase 1 (HO-1)-dependent pathway. Doxorubicin 0-11 heme oxygenase 1 Homo sapiens 157-173 30159756-1 2018 Doxorubicin (Dox)-induced cardiotoxicity, a limiting factor in the use of Dox to treat cancer, can be mitigated by the mitogenic factor FGF2 in vitro, via a heme oxygenase 1 (HO-1)-dependent pathway. Doxorubicin 0-11 heme oxygenase 1 Homo sapiens 175-179 30159756-1 2018 Doxorubicin (Dox)-induced cardiotoxicity, a limiting factor in the use of Dox to treat cancer, can be mitigated by the mitogenic factor FGF2 in vitro, via a heme oxygenase 1 (HO-1)-dependent pathway. Doxorubicin 0-3 heme oxygenase 1 Homo sapiens 157-173 30159756-1 2018 Doxorubicin (Dox)-induced cardiotoxicity, a limiting factor in the use of Dox to treat cancer, can be mitigated by the mitogenic factor FGF2 in vitro, via a heme oxygenase 1 (HO-1)-dependent pathway. Doxorubicin 0-3 heme oxygenase 1 Homo sapiens 175-179 30159756-1 2018 Doxorubicin (Dox)-induced cardiotoxicity, a limiting factor in the use of Dox to treat cancer, can be mitigated by the mitogenic factor FGF2 in vitro, via a heme oxygenase 1 (HO-1)-dependent pathway. Doxorubicin 13-16 heme oxygenase 1 Homo sapiens 157-173 30159756-1 2018 Doxorubicin (Dox)-induced cardiotoxicity, a limiting factor in the use of Dox to treat cancer, can be mitigated by the mitogenic factor FGF2 in vitro, via a heme oxygenase 1 (HO-1)-dependent pathway. Doxorubicin 13-16 heme oxygenase 1 Homo sapiens 175-179 29541348-0 2018 Protective Effect of Boswellic Acids against Doxorubicin-Induced Hepatotoxicity: Impact on Nrf2/HO-1 Defense Pathway. Doxorubicin 45-56 heme oxygenase 1 Homo sapiens 96-100 29541348-8 2018 BAs increased the Nrf2 and HO-1 expression, which provided protection against DOX-induced oxidative insult. Doxorubicin 78-81 heme oxygenase 1 Homo sapiens 27-31 31356549-0 2019 Curdione Ameliorated Doxorubicin-Induced Cardiotoxicity Through Suppressing Oxidative Stress and Activating Nrf2/HO-1 Pathway. Doxorubicin 21-32 heme oxygenase 1 Homo sapiens 113-117 31356549-9 2019 Further study indicated that curdione decreased DOX-induced phosphorylation of extracellular signal-regulated kinase1/2 (Erk1/2) and c-Jun-N-terminal kinase and activated nuclear factor-erythroid 2-related factor 2/heme oxygenase 1 (Nrf2/HO-1) signal pathway. Doxorubicin 48-51 heme oxygenase 1 Homo sapiens 238-242 31679277-0 2019 Nrf2/HO-1 Mediated Protective Activity of Genistein Against Doxorubicin-Induced Cardiac Toxicity. Doxorubicin 60-71 heme oxygenase 1 Homo sapiens 5-9 29152091-0 2017 Fibroblast growth factor-2-mediated protection of cardiomyocytes from the toxic effects of doxorubicin requires the mTOR/Nrf-2/HO-1 pathway. Doxorubicin 91-102 heme oxygenase 1 Homo sapiens 127-131 29152091-9 2017 Conclusions: In an acute setting Hi- or Lo-FGF-2 protect cardiomyocytes against multiple Dox-induced deleterious effects, by a mechanism dependent on preservation of mTOR activity, Nrf-2 levels, and the upregulation of HO-1. Doxorubicin 89-92 heme oxygenase 1 Homo sapiens 219-223 26058377-11 2016 In conclusion, our results indicate that a new DSS derivative exhibits promising protective effects against Dox-induced cardiotoxicity both in vivo and in vitro, an effect at least partially mediated by induction of HO-1 expression and the activation of mitochondrial biogenesis. Doxorubicin 108-111 heme oxygenase 1 Homo sapiens 216-220 27110594-4 2016 Relative to WT mice, mice globally overexpressing human HO-1 were protected from DOX-induced dilated cardiomyopathy, cardiac cytoarchitectural derangement, and infiltration of CD11b+ mononuclear phagocytes. Doxorubicin 81-84 heme oxygenase 1 Homo sapiens 56-60 26227317-10 2015 Xenograft studies showed that HO-1 regulation by doxorubicin also occurs in vivo. Doxorubicin 49-60 heme oxygenase 1 Homo sapiens 30-34 26227317-11 2015 Immunofluorescence analysis revealed that BRCA1 overexpression and/or doxorubicin exposure induced the cytoplasmic retention of HO-1. Doxorubicin 70-81 heme oxygenase 1 Homo sapiens 128-132 26722274-0 2015 Knockdown of heme oxygenase-1 promotes apoptosis and autophagy and enhances the cytotoxicity of doxorubicin in breast cancer cells. Doxorubicin 96-107 heme oxygenase 1 Homo sapiens 13-29 26722274-2 2015 In the present study, HMOX-1 was demonstrated to be overexpressed and able to be induced by doxorubicin in breast cancer cell lines. Doxorubicin 92-103 heme oxygenase 1 Homo sapiens 22-28 26722274-3 2015 Knockdown of HMOX-1 using short interfering (si)RNA enhanced the cytotoxicity of doxorubicin in MDA-MB-231 and BT549 cells. Doxorubicin 81-92 heme oxygenase 1 Homo sapiens 13-19 26722274-4 2015 Knockdown of HMOX-1 downregulated B cell lymphoma (Bcl)-2 and Bcl-extra large expression, and significantly enhanced doxorubicin-induced apoptosis in MDA-MB-231 and BT549 cells. Doxorubicin 117-128 heme oxygenase 1 Homo sapiens 13-19 26722274-5 2015 Additionally, knockdown of HMOX-1 upregulated light chain 3B expression and markedly increased the accumulation of autophagic vacuoles in MDA-MB-231 and BT549 cells treated with doxorubicin. Doxorubicin 178-189 heme oxygenase 1 Homo sapiens 27-33 26722274-7 2015 Therefore, HMOX-1 may represent a potential therapeutic target for enhancing the cytotoxicity and efficacy of doxorubicin during the treatment of breast cancer. Doxorubicin 110-121 heme oxygenase 1 Homo sapiens 11-17 26041409-3 2015 In the present study, we found an induction of HO-1 expression in doxorubicin (DOX)-treated MDA-MB-231 human breast adenocarcinoma cells, which showed insensitivity to DOX treatment. Doxorubicin 66-77 heme oxygenase 1 Homo sapiens 47-51 26041409-3 2015 In the present study, we found an induction of HO-1 expression in doxorubicin (DOX)-treated MDA-MB-231 human breast adenocarcinoma cells, which showed insensitivity to DOX treatment. Doxorubicin 79-82 heme oxygenase 1 Homo sapiens 47-51 26041409-4 2015 Knockdown HO-1 expression dramatically upregulated the incidence of MDA-MB-231 cell death under DOX treatment, indicating that HO-1 functions as a critical contributor to drug resistance in MDA-MB-231 cells. Doxorubicin 96-99 heme oxygenase 1 Homo sapiens 10-14 26041409-4 2015 Knockdown HO-1 expression dramatically upregulated the incidence of MDA-MB-231 cell death under DOX treatment, indicating that HO-1 functions as a critical contributor to drug resistance in MDA-MB-231 cells. Doxorubicin 96-99 heme oxygenase 1 Homo sapiens 127-131 26041409-5 2015 We further observed that DOX exposure induced a cytoprotective autophagic flux in MDA-MB-231 cells, which was dependent on HO-1 induction. Doxorubicin 25-28 heme oxygenase 1 Homo sapiens 123-127 26041409-8 2015 Therefore, we conclude that Src/STAT3-dependent HO-1 induction protects MDA-MB-231 breast cancer cells from DOX-induced death through promoting autophagy. Doxorubicin 108-111 heme oxygenase 1 Homo sapiens 48-52 26041409-9 2015 In the following study, we further demonstrated the contribution of Src/STAT3/HO-1/autophagy pathway activation to DOX resistance in another breast cancer cell line, MDA-MB-468, which bears a similar phenotype to MDA-MB-231 cells. Doxorubicin 115-118 heme oxygenase 1 Homo sapiens 78-82 26041409-10 2015 Therefore, activation of Src/STAT3/HO-1/autophagy signaling pathway might play a general role in protecting certain subtypes of breast cancer cells from DOX-induced cytotoxicity. Doxorubicin 153-156 heme oxygenase 1 Homo sapiens 35-39 35422894-0 2022 Choline Protects the Heart from Doxorubicin-Induced Cardiotoxicity through Vagal Activation and Nrf2/HO-1 Pathway. Doxorubicin 32-43 heme oxygenase 1 Homo sapiens 101-105 22593043-3 2013 We found that the endogenous expression of Nrf2 as well as its target proteins heme oxygenase-1 (HO-1), NADP(H):quinone oxidoreductase (NQO) in MCF-7/DOX cells was higher than that in MCF-7 cells. Doxorubicin 150-153 heme oxygenase 1 Homo sapiens 79-95 22593043-3 2013 We found that the endogenous expression of Nrf2 as well as its target proteins heme oxygenase-1 (HO-1), NADP(H):quinone oxidoreductase (NQO) in MCF-7/DOX cells was higher than that in MCF-7 cells. Doxorubicin 150-153 heme oxygenase 1 Homo sapiens 97-101 20733275-7 2010 In in vitro experiments using urothelial cancer cell lines, HO-1 upregulation was observed by exposure to doxorubicin. Doxorubicin 106-117 heme oxygenase 1 Homo sapiens 60-64 20733275-8 2010 Moreover, siRNA-mediated suppression of HO-1 upregulation sensitized the urothelial cancer cells to doxorubicin. Doxorubicin 100-111 heme oxygenase 1 Homo sapiens 40-44 17140381-0 2006 Changes in expression of genes encoding antioxidant enzymes, heme oxygenase-1, Bcl-2, and Bcl-xl and in level of reactive oxygen species in tumor cells resistant to doxorubicin. Doxorubicin 165-176 heme oxygenase 1 Homo sapiens 61-77 18845130-0 2009 Reactive oxygen species-independent apoptosis in doxorubicin-treated H9c2 cardiomyocytes: role for heme oxygenase-1 down-modulation. Doxorubicin 49-60 heme oxygenase 1 Homo sapiens 99-115 35422894-5 2022 Levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme-oxygenase-1 (HO-1), which are antioxidant markers, were lowered by DOX and upregulated by choline. Doxorubicin 137-140 heme oxygenase 1 Homo sapiens 65-81 35422894-5 2022 Levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme-oxygenase-1 (HO-1), which are antioxidant markers, were lowered by DOX and upregulated by choline. Doxorubicin 137-140 heme oxygenase 1 Homo sapiens 83-87 33923922-8 2021 These were effectively antagonized with MGN (20 muM), which led to HUVECs being protected against DOX-induced apoptosis, partly through the PI3K/AKT-mediated NRF2/HO-1 signaling pathway, which could theoretically protect the vessels from severe DOX toxicity. Doxorubicin 98-101 heme oxygenase 1 Homo sapiens 163-167