ArticleFrontiers in oncology2025
Overexpression of BNIP3 in renal carcinoma cells can promote apoptosis of renal carcinoma cells through HIF-1α-BNIP3-mediated autophagy.
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Exploring regulated cell death in renal cell carcinoma: mechanistic insights and therapeutic perspectives.Apoptosis : an international journal on programmed cell death · 2026Review
- Mitochondrial Transplantation Rejuvenates Aging Heart by Restoring Mitophagy Flux via the HIF-3α-BNIP3 Axis.Aging cell · 2026Article
- Mitochondrial Dysfunction in Renal Cell Carcinoma: A Comprehensive Review of Pathogenic Mechanisms and Emerging Therapeutic Opportunities.Oncology research · 2026Review
- 1,8-Cineole improves hepatic fibrosis by inhibiting HIF-1α/BNIP3/PINK1/Parkin-dependent mitophagy signaling and inducing apoptosis in activated hepatic stellate cells.Frontiers in pharmacology · 2026Article
- Mitophagy's impacts on cancer and neurodegenerative diseases: implications for future therapies.Journal of hematology & oncology · 2025Review
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12 authors.
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Abstract
Background: Renal cell carcinoma (RCC) is a prevalent malignancy with limited effective therapies, necessitating novel molecular targets. BNIP3, a pro-apoptotic protein regulated by hypoxia-inducible factor 1 (HIF-1), is implicated in autophagy and apoptosis, but its role in RCC under hypoxic conditions remains underexplored. This study investigates the effects of BNIP3 overexpression on RCC cell behavior and its molecular mechanisms. Methods: Human RCC cell lines A498 and 786-O were transfected with pcDNA3.1-BNIP3 to overexpress BNIP3 and cultured under normoxic (21% O Results: BNIP3 overexpression significantly reduced proliferation and invasion while increasing apoptosis in A498 and 786-O cells (P<0.01). Under hypoxia, BNIP3 disrupted the Bcl-2/Beclin1 complex, enhancing autophagy by increasing LC3B and autophagosome formation and decreasing p62 (P<0.01). Autophagy inhibitor 3-MA suppressed BNIP3-induced apoptosis, indicating autophagy-dependent apoptosis. Conclusion: BNIP3 overexpression inhibits RCC progression by promoting HIF-1α-mediated autophagy and subsequent apoptosis under hypoxic conditions, primarily through disrupting the Bcl-2/Beclin1 complex. These findings establish BNIP3 as a potential therapeutic target for RCC, warranting further investigation into autophagy-based interventions.
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