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Article Publish Status: FREE
Abstract Title:

In vitro and in vivo study of epigallocatechin-3-gallate-induced apoptosis in aerobic glycolytic hepatocellular carcinoma cells involving inhibition of phosphofructokinase activity.

Abstract Source:

Sci Rep. 2016 ;6:28479. Epub 2016 Jun 28. PMID: 27349173

Abstract Author(s):

Sainan Li, Liwei Wu, Jiao Feng, Jingjing Li, Tong Liu, Rong Zhang, Shizan Xu, Keran Cheng, Yuqing Zhou, Shunfeng Zhou, Rui Kong, Kan Chen, Fan Wang, Yujing Xia, Jie Lu, Yingqun Zhou, Weiqi Dai, Chuanyong Guo

Article Affiliation:

Sainan Li

Abstract:

Glycolysis, as an altered cancer cell-intrinsic metabolism, is an essential hallmark of cancer. Phosphofructokinase (PFK) is a metabolic sensor in the glycolytic pathway, and restricting the substrate availability for this enzyme has been researched extensively as a target for chemotherapy. In the present study, we investigated that the effects of epigallocatechin-3-gallate (EGCG), an active component of green tea, on inhibiting cell growth and inducing apoptosis by promoting a metabolic shift away from glycolysis in aerobic glycolytic hepatocellular carcinoma (HCC) cells. EGCG modulated the oligomeric structure of PFK, potentially leading to metabolic stress associated apoptosis and suggesting that EGCG acts by directly suppressing PFK activity. A PFK activity inhibitor enhanced the effect, while the allosteric activator reversed EGCG-induced HCC cell death. PFK siRNA knockdown-induced apoptosis was not reversed by the activator. EGCG enhanced the effect of sorafenib on cell growth inhibition in both aerobic glycolytic HCC cells and in a xenograft mouse model. The present study suggests a potential role for EGCG as an adjuvant in cancer therapy, which merits further investigation at the clinical level.

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