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Peer-reviewedCC BY-NC-NDCurrent urology

Targeting lipid metabolism to overcome therapeutic resistance in renal cell carcinoma: Mechanisms and emerging strategies.

  1. 1Department of Urology, Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Tianjin, China.
  2. 2Department of Microbiology, School of Medical Laboratory, Tianjin Medical University, Tianjin, China.

Abstract

Renal cell carcinoma (RCC) is a common urological cancer. Despite advances in immunotherapy and targeted therapy, drug resistance profoundly compromises outcomes. Aberrant lipid metabolism critically shapes the tumor microenvironment and fosters resistance via diverse mechanisms, although the precise underlying pathological pathways remain unclear. This review provides current insights and highlights emerging trends to guide future research. Research interest in the role of lipid metabolism in therapeutic resistance in renal cancer has steadily increased over the years. Lipid metabolism influences therapeutic resistance in RCC primarily through the protein kinase B/mechanistic target of rapamycin signaling pathway, ferroptosis, autophagy, synergy with glucose metabolism, and drug efflux mechanisms. Identifying lipid metabolism biomarkers that are predictive of RCC treatment response and multi-integrating multiomics approaches to optimize therapeutic strategies are critical directions for future studies. Targeting lipid metabolism represents a pivotal nexus between targeted therapy and immunotherapy. Elucidating its interplay with programmed cell death pathways, including ferroptosis and autophagy, may help overcome resistance in RCC. However, the reliance on preclinical models limits their clinical translation. This review refines the current knowledge, identifies emerging avenues, and offers guidance for future research.

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BibTeX
@article{feng2026targeting,
  title = {{Targeting lipid metabolism to overcome therapeutic resistance in renal cell carcinoma: Mechanisms and emerging strategies.}},
  author = {Yuankang Feng and Shiyue Zhang and Jianqiao Li and Dan Yue and Yong Wang},
  journal = {Current urology},
  year = {2026},
  month = may,
  doi = {10.1097/cu9.0000000000000355},
  url = {https://europepmc.org/article/MED/42960049},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Targeting lipid metabolism to overcome therapeutic resistance in renal cell carcinoma: Mechanisms and emerging strategies.
AU  - Yuankang Feng
AU  - Shiyue Zhang
AU  - Jianqiao Li
AU  - Dan Yue
AU  - Yong Wang
PY  - 2026
DA  - 2026/05/12
JO  - Current urology
DO  - 10.1097/cu9.0000000000000355
UR  - https://europepmc.org/article/MED/42960049
AB  - Renal cell carcinoma (RCC) is a common urological cancer. Despite advances in immunotherapy and targeted therapy, drug resistance profoundly compromises outcomes. Aberrant lipid metabolism critically shapes the tumor microenvironment and fosters resistance via diverse mechanisms, although the precise underlying pathological pathways remain unclear. This review provides current insights and highlights emerging trends to guide future research. Research interest in the role of lipid metabolism in therapeutic resistance in renal cancer has steadily increased over the years. Lipid metabolism influences therapeutic resistance in RCC primarily through the protein kinase B/mechanistic target of rapamycin signaling pathway, ferroptosis, autophagy, synergy with glucose metabolism, and drug efflux mechanisms. Identifying lipid metabolism biomarkers that are predictive of RCC treatment response and multi-integrating multiomics approaches to optimize therapeutic strategies are critical directions for future studies. Targeting lipid metabolism represents a pivotal nexus between targeted therapy and immunotherapy. Elucidating its interplay with programmed cell death pathways, including ferroptosis and autophagy, may help overcome resistance in RCC. However, the reliance on preclinical models limits their clinical translation. This review refines the current knowledge, identifies emerging avenues, and offers guidance for future research.
SN  - 1661-7649
SN  - 1661-7657
ER  -