ArticleOncotarget2017
HMGB1-mediated autophagy attenuates gemcitabine-induced apoptosis in bladder cancer cells involving JNK and ERK activation.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 82 citations in OpenAlex.
- Pathophysiological significance of the TRPM2 ion channel as a potential target in cancer, neurological disorders, and ischemia/reperfusion injury.Pharmacological research · 2026Review
- From molecular networks to translational intervention: current progress in the mechanisms of gemcitabine resistance in bladder cancer.Frontiers in immunology · 2026Review
- HMGB1 as Double-Edged Regulator of Cancer Therapy: Mechanistic Roles in Chemotherapy Resistance and Immunotherapy Response.OncoTargets and therapy · 2026Review
- Ursolic acid sensitizes bladder cancer to gemcitabine chemotherapy by concurrently targeting PI3K/AKT and JNK pathways.Translational andrology and urology · 2025Article
- Independent and interactive roles of hirudin and HMGB1 interference in protecting renal function by regulating autophagy, apoptosis, and kidney injury in chronic kidney disease.European journal of histochemistry : EJH · 2025Article
- Inhibitory effects of the combination of rapamycin with gemcitabine plus paclitaxel on the growth of pancreatic cancer tumors.Human cell · 2025Article
- Therapeutic importance and diagnostic function of circRNAs in urological cancers: from metastasis to drug resistance.Cancer metastasis reviews · 2024Review
- The role of programmed cell death in osteosarcoma: From pathogenesis to therapy.Cancer medicine · 2024Review
- Deciphering the impact of circRNA-mediated autophagy on tumor therapeutic resistance: a novel perspective.Cellular & molecular biology letters · 2024Review
- Ubiquitin-specific protease 5 promotes bladder cancer progression through stabilizing Twist1.Oncogene · 2024Article
- Multiple functions of HMGB1 in cancer.Frontiers in oncology · 2024Review
- Ischemic postconditioning protects against acute kidney injury after limb ischemia reperfusion by regulating HMGB1 release and autophagy.Renal failure · 2023Article
- WTAP regulates autophagy in colon cancer cells by inhibiting FLNA through N6-methyladenosine.Cell adhesion & migration · 2023Article
- Therapeutic effects of medicinal plants and their constituents on lung cancer, in vitro, in vivo and clinical evidence.Journal of cellular and molecular medicine · 2023Review
- Glycyrrhizin, an inhibitor of HMGB1 induces autolysosomal degradation function and inhibits Helicobacter pylori infection.Molecular medicine (Cambridge, Mass.) · 2023Article
- Resistance to Gemcitabine in Pancreatic Ductal Adenocarcinoma: A Physiopathologic and Pharmacologic Review.Cancers · 2022Review
- EGF-induced nuclear translocation of SHCBP1 promotes bladder cancer progression through inhibiting RACGAP1-mediated RAC1 inactivation.Cell death & disease · 2022Article
- Extracellular HMGB1 interacts with RAGE and promotes chemoresistance in acute leukemia cells.Cancer cell international · 2021Article
- Exosomal HMGB1 derived from hypoxia-conditioned bone marrow mesenchymal stem cells increases angiogenesis via the JNK/HIF-1α pathway.FEBS open bio · 2021Article
- Molecular imaging of the kinetics of hyperactivated ERK1/2-mediated autophagy during acquirement of chemoresistance.Cell death & disease · 2021Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High-mobility group box 1 (HMGB1) has been found to mediate autophagy during chemotherapy in several cancers. However, whether HMGB1plays a role in autophagy and chemoresistance in bladder cancer is elusive. In this report, HMGB1 expression was found to be increased in 30 primary bladder cancer tissue specimens compared to their matched adjacent non-tumor tissues. While gemcitabine induced apoptotic cell death, it also induced HMGB1 expression and autophagy in bladder cancer T24 and BIU-87 cells. Suppressing HMGB1 expression with siRNA strongly potentiated gemcitabine-induced apoptosis. HMGB1 siRNA or autophagy inhibitors suppressed gemcitabine-induced autophagy. Further, gemcitabine activated c-Jun N-terminal kinase (JNK) and extracellular regulated protein kinase (ERK) and Bcl-2 phosphorylation, and blocking ERK and JNK inhibited autophagy and increased apoptosis in gemcitabine-treated cells. Interestingly, suppressing HMGB1 expression attenuated gemcitabine-induced ERK and JNK activation and Bcl-2 phosphorylation. Thus, our results suggest that while gemcitabine kills bladder cancer cells through apoptosis, a cytoprotective autophagy is also induced involving HMGB1-mediated JNK and ERK to counteract the cytotoxicity of gemcitabine, and intervention targeting this pathway may improve the anticancer efficacy of gemcitabine against bladder cancer.
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