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Review
. 2022 Mar;41(1):17-31.
doi: 10.1007/s10555-021-09996-w. Epub 2021 Nov 6.

Lipid metabolism reprogramming in renal cell carcinoma

Gioia Heravi  1 , Omid Yazdanpanah  2 , Izabela Podgorski  3   4   5 , Larry H Matherly  3   4   5 , Wanqing Liu  6   7   8   9
Affiliations
Review

Lipid metabolism reprogramming in renal cell carcinoma

Gioia Heravi et al. Cancer Metastasis Rev. 2022 Mar.

Abstract

Metabolic reprogramming is recognized as a hallmark of cancer. Lipids are the essential biomolecules required for membrane biosynthesis, energy storage, and cell signaling. Altered lipid metabolism allows tumor cells to survive in the nutrient-deprived environment. However, lipid metabolism remodeling in renal cell carcinoma (RCC) has not received the same attention as in other cancers. RCC, the most common type of kidney cancer, is associated with almost 15,000 death in the USA annually. Being refractory to conventional chemotherapy agents and limited available targeted therapy options has made the treatment of metastatic RCC very challenging. In this article, we review recent findings that support the importance of synthesis and metabolism of cholesterol, free fatty acids (FFAs), and polyunsaturated fatty acids (PUFAs) in the carcinogenesis and biology of RCC. Delineating the detailed mechanisms underlying lipid reprogramming can help to better understand the pathophysiology of RCC and to design novel therapeutic strategies targeting this malignancy.

Keywords: Cholesterol; Free fatty acids; Metabolic reprogramming; PUFA; Renal cell carcinoma.

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Conflict of interest statement

Conflict of interest The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Lipid metabolism. Acetyl-CoA is the starting material in cholesterol and FFA biosynthesis. Cholesterol and FFA can also be provided from exogenous resources. The red boxes are the proteins involved in lipid regulation
Fig. 2
Fig. 2
PUFA metabolism pathway. Linoleic acid and α-Linolenic acid are the essential PUFA provided from food. Other PUFA can either be obtained from diet or synthesized in the body. Blue boxes represent the enzymes involved in PUFA metabolism
Fig. 3
Fig. 3
HIF pathway in ccRCC. VHL mutation, mTOR activation, and hypoxia cause an increase of HIFs in the cell. This event ultimately leads to LD accumulation
See this image and copyright information in PMC

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