Targeting at cancer energy metabolism and lipid droplet formation as new treatment strategies for epigallocatechin-3-gallate (EGCG) in colorectal cancer cells

被引：16

作者：

Wang, Yujie ^{[1
]}

Pan, Haitao ^{[1
]}

Chen, Dian ^{[1
]}

Guo, Dandan ^{[1
]}

Wang, Xingya ^{[1
]}

机构：

[1] Zhejiang Chinese Med Univ, Coll Pharmaceut Sci, 260 Baichuan Rd, Hangzhou 311400, Peoples R China

来源：

JOURNAL OF FUNCTIONAL FOODS | 2021年 / 83卷

基金：

中国国家自然科学基金;

关键词：

EGCG; Lipid droplet; Fatty acid de novo synthesis; Energy metabolism; AMPK; Colorectal cancer; ACETYL-COA-CARBOXYLASE; FATTY-ACID-METABOLISM; ACTIVATED PROTEIN-KINASE; GREEN TEA; PHOSPHORYLATION SITES; SYNTHASE; PREVENTION; OXIDATION; WEIGHT; ROLES;

D O I：

10.1016/j.jff.2021.104570

中图分类号：

TS2 [食品工业];

学科分类号：

0832 ;

摘要：

Fatty acid metabolic reprogramming is an important hallmark of cancer cells. In this study, we examined the effects of the green tea polyphenol EGCG on fatty acid and energy metabolisms in colorectal cancer (CRC) cells. EGCG significantly inhibited the viability of HCT116 and HT-29 cancer cells, accompanied by decreased lipid droplet formation and triglyceride contents. EGCG deregulated the expression of the key genes involved in fatty acid de novo synthesis, lipid uptake, lipolysis, fatty acid beta oxidation, and thermogenesis at both the mRNA and protein levels. Besides, EGCG decreased the mitochondrial oxygen consumption rate (OCR), cytosolic glycolysis, and ATP production in CRC cells. Moreover, EGCG activated AMPK in CRC cells, whereas AMPK inhibitor Compound C increased the cell viability, expression of FASN, and lipid droplet formation in HCT116 cells when cotreated with EGCG. Collectively, EGCG may serve as a potent fatty acid and energy metabolism regulator to inhibit CRC.

引用

页数：15

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