Adipocyte and lipid metabolism in cancer drug resistance

被引:360
作者
Cao, Yihai [1 ]
机构
[1] Karolinska Inst, Dept Microbiol Tumor & Cell Biol, Stockholm, Sweden
基金
瑞典研究理事会; 欧洲研究理事会;
关键词
PROMOTE TUMOR PROGRESSION; FATTY-ACID OXIDATION; BODY-MASS INDEX; ADIPOSE-TISSUE; PROSTATE-CANCER; COLORECTAL-CANCER; CELL RESISTANCE; BINDING PROTEIN; OBESITY; GROWTH;
D O I
10.1172/JCI127201
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Development of novel and effective therapeutics for treating various cancers is probably the most congested and challenging enterprise of pharmaceutical companies. Diverse drugs targeting malignant and nonmalignant cells receive clinical approval each year from the FDA. Targeting cancer cells and nonmalignant cells unavoidably changes the tumor microenvironment, and cellular and molecular components relentlessly alter in response to drugs. Cancer cells often reprogram their metabolic pathways to adapt to environmental challenges and facilitate survival, proliferation, and metastasis. While cancer cells' dependence on glycolysis for energy production is well studied, the roles of adipocytes and lipid metabolic reprogramming in supporting cancer growth, metastasis, and drug responses are less understood. This Review focuses on emerging mechanisms involving adipocytes and lipid metabolism in altering the response to cancer treatment. In particular, we discuss mechanisms underlying cancer-associated adipocytes and lipid metabolic reprogramming in cancer drug resistance.
引用
收藏
页码:3006 / 3017
页数:12
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