Obesity-Related Mechanisms in Renal Cell Carcinoma
Summary
Obesity is a well-established risk factor for renal cell carcinoma, the predominant form of kidney cancer. Excess energy intake and expanded adipose tissue foster tumour initiation and progression through metabolic dysregulation, chronic inflammation and hypoxia. Adipocytes release a spectrum of bioactive molecules, or adipokines, that modulate insulin resistance, oxidative stress and immune cell recruitment in the renal microenvironment. These perturbations activate central signalling cascades—PI3K–AKT–mTOR, AMPK and WNT–β-catenin—that drive cellular proliferation, angiogenesis and survival. Concurrently, epigenetic alterations such as DNA methylation, histone modification and aberrant microRNA expression reshape gene networks to favour oncogenesis. Direct interactions between perinephric adipose tissue and tumour cells further enhance invasive behaviour via paracrine WNT ligands and inflammatory mediators. Notably, an “obesity paradox” has emerged, whereby higher body mass index may correlate with improved survival, possibly reflecting altered adipokine profiles and immune modulation. A comprehensive understanding of these interwoven mechanisms is crucial to developing novel biomarkers and targeted interventions for obesity-associated renal malignancies.
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Obesity-Related Mechanisms in Renal Cell Carcinoma publication trend
The graph below shows the total number of articles in obesity-related mechanisms in renal cell carcinoma across all publications each year (not limited to Nature Index journals).
Technical terms
Adipokine: Signalling proteins secreted by adipose tissue that regulate metabolism and inflammation.
Adiponectin: An adipokine with insulin-sensitising and anti-inflammatory actions, typically reduced in obesity.
MicroRNA (miRNA): Small non-coding RNAs that bind messenger RNA to inhibit translation or promote degradation.
Perinephric adipose tissue: Fat immediately surrounding the kidney that communicates with tumour cells via paracrine factors.
PI3K–AKT–mTOR pathway: A signalling cascade that integrates nutrient and growth signals to control cell growth and survival.
References
- Renal Cell Cancer and Obesity. International Journal of Molecular Sciences (2022).
- Low adiponectin levels are associated with renal cell carcinoma: A case‐control study. International Journal of Cancer (2007).
- The impact of obesity and adiponectin signaling in patients with renal cell carcinoma: A potential mechanism for the “obesity paradox”. PLOS ONE (2017).
- Potential Value of Visfatin, Omentin-1, Nesfatin-1 and Apelin in Renal Cell Carcinoma (RCC): A Systematic Review and Meta-Analysis. Diagnostics (2022).
- Effect of perineoplasm perinephric adipose tissues on migration of clear cell renal cell carcinoma cells: a potential role of WNT signaling. Oncotarget (2016).
- Heterogeneous miRNA-mRNA Regulatory Networks of Visceral and Subcutaneous Adipose Tissue in the Relationship Between Obesity and Renal Clear Cell Carcinoma. Frontiers in Endocrinology (2021).
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