ORIGINAL RESEARCH article
Front. Oncol.
Sec. Genitourinary Oncology
Volume 15 - 2025 | doi: 10.3389/fonc.2025.1614378
This article is part of the Research TopicKidney Cancer Awareness Month 2025: Current Progress and Future Prospects on Kidney Cancer Prevention, Diagnosis and TreatmentView all 4 articles
Overexpression of BNIP3 in renal carcinoma cells can promote apoptosis of renal carcinoma cells through HIF-1α-BNIP3mediated autophagy
Provisionally accepted
Long Huang*
Lin WangDan YuanYan XuYu Wang
Yao KaiXiao ZhongQuanda LiuJia KangLei LeiHaiyan Wang
Dongliang Liu*- Department of Urology, AVIC 363 Hospital, Chengdu, China
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This research delved into the intricate role of BNIP3 (Bcl-2/adenovirus E1B 19 kDa interacting protein 3) overexpression in the biological processes of renal cell carcinoma (RCC), specifically its functions in mediating autophagy and promoting apoptosis, and sought to uncover the underlying molecular mechanism. Initial observations indicated that the up-regulation of BNIP3 led to a significant decrease in the proliferation and invasion capabilities of RCC cells. This reduction in malignancy-related behaviors was accompanied by an increase in the apoptosis rate of these cells, suggesting a potential anti-tumor effect of BNIP3 overexpression. Under hypoxic conditions, a microenvironmental factor often associated with tumor progression, BNIP3 played a crucial role. It disrupted the interaction between Bcl-2 and Beclin1, which is a key step in the initiation of autophagy. This disruption triggered autophagy activation in RCC cells. Moreover, this autophagy activation was found to have a direct link with apoptosis. The autophagic process induced by BNIP3 served as a driving force for apoptosis, thereby accelerating the progression of tumorigenesis in the in vivo models. Collectively, these findings offer substantial evidence that BNIP3 overexpression can suppress tumor growth under hypoxic conditions. By inducing autophagy and facilitating apoptosis in RCC cells, BNIP3 presents a promising avenue for the development of novel therapeutic strategies.These results not only enhance our understanding of the molecular basis of RCC but also identify potential targets for more effective therapeutic interventions against this disease.
Keywords: Renal cell carcinoma, BNIP3, B-cell lymphoma-2, HIF-1α, Autophagy, Apoptosis
Received: 18 Apr 2025; Accepted: 21 Jul 2025.
Copyright: © 2025 Huang, Wang, Yuan, Xu, Wang, Kai, Zhong, Liu, Kang, Lei, Wang and Liu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Long Huang, Department of Urology, AVIC 363 Hospital, Chengdu, China
Dongliang Liu, Department of Urology, AVIC 363 Hospital, Chengdu, China
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