Role of Metabolic Reprogramming in Epithelial-Mesenchymal Transition (EMT)

被引:102
作者
Kang, Hyunkoo [1 ]
Kim, Hyunwoo [1 ]
Lee, Sungmin [1 ]
Youn, HyeSook [2 ]
Youn, BuHyun [1 ,3 ]
机构
[1] Pusan Natl Univ, Dept Integrated Biol Sci, Busan 46241, South Korea
[2] Sejong Univ, Dept Integrat Biosci & Biotechnol, Seoul 05006, South Korea
[3] Pusan Natl Univ, Dept Biol Sci, Busan 46241, South Korea
基金
新加坡国家研究基金会;
关键词
metabolic reprogramming; EMT; metastasis; cancer progression; FATTY-ACID SYNTHASE; BREAST-CANCER CELLS; PYRUVATE-KINASE M2; PROSTATE-CANCER; HEPATOCELLULAR-CARCINOMA; LUNG-CANCER; GLUTAMINE-METABOLISM; SIGNALING PATHWAY; IDH2; MUTATIONS; OVARIAN-CANCER;
D O I
10.3390/ijms20082042
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Activation of epithelial-mesenchymal transition (EMT) is thought to be an essential step for cancer metastasis. Tumor cells undergo EMT in response to a diverse range of extra- and intracellular stimulants. Recently, it was reported that metabolic shifts control EMT progression and induce tumor aggressiveness. In this review, we summarize the involvement of altered glucose, lipid, and amino acid metabolic enzyme expression and the underlying molecular mechanisms in EMT induction in tumor cells. Moreover, we propose that metabolic regulation through gene-specific or pharmacological inhibition may suppress EMT and this treatment strategy may be applied to prevent tumor progression and improve anti-tumor therapeutic efficacy. This review presents evidence for the importance of metabolic changes in tumor progression and emphasizes the need for further studies to better understand tumor metabolism.
引用
收藏
页数:21
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