Abstract
Lipid metabolism reprograming, as a hallmark of malignancy, has received renewed interest in recent years in such areas as energy sources, cell membrane components, and signaling molecules involved in the rapid tumor growth and the adaptation to the tumor microenvironment. Lipid metabolism deregulation in cancer involves multiple aspects, including an increased lipid uptake, endogenous de novo fatty acid synthesis, fatty acid oxidation, and cholesterol accumulation, thereby promoting tumor growth and progression. Recent advances in the understanding of specific metabolic alterations in cancer reveal novel pathogenesis mechanisms and a growing number of drugs targeting lipid metabolism have been applied in anti-tumor therapy. Thus, this review discusses the lipid metabolic landscape of cancers and the interplay with oncogenic signaling, and summarizes potential therapeutic targets to improve the therapeutic efficiency in cancer patients, in order to provide more reference and thinking for the treatment of lipid metabolism of cancer patients.
Highlights
Lipid metabolism reprograming is a hallmark of cancer and plays an important role in shaping the tumor microenvironment and cancer cell phenotype, contributing to the occurrence and development of tumors [1]
Since cancer cells compete for oxygen and nutrients in a nutrient-limited microenvironment, they maintain their malignant potential by altering their metabolism and obtaining fatty acids (FAs)
Aktdependent lipogenesis requires a mammalian target of rapamycin activity to regulate SREBP1 activity, inducing the increased expression of enzymes involved in lipid biosynthesis, including ATP-citrate lyase (ACLY), fatty acid synthase (FASN), and acetyl-CoA carboxylase (ACC) [30]
Summary
Lipid metabolism reprograming is a hallmark of cancer and plays an important role in shaping the tumor microenvironment and cancer cell phenotype, contributing to the occurrence and development of tumors [1]. Cancer cells rewire lipid metabolism through several mechanisms, including increased de novo synthesis and exogenous uptake of FAs, upregulated fatty acid oxidation (FAO), cholesterol accumulation, and induced cancer-associated adipose tissue.
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