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Abstract Title:

PKM2 is the target of proanthocyanidin B2 during the inhibition of hepatocellular carcinoma.

Abstract Source:

J Exp Clin Cancer Res. 2019 May 17 ;38(1):204. Epub 2019 May 17. PMID: 31101057

Abstract Author(s):

Jiao Feng, Liwei Wu, Jie Ji, Kan Chen, Qiang Yu, Jie Zhang, Jiaojiao Chen, Yuqing Mao, Fan Wang, Weiqi Dai, Ling Xu, Jianye Wu, Chuanyong Guo

Article Affiliation:

Jiao Feng

Abstract:

BACKGROUND: The treatment for advanced primary hepatocellular carcinoma (HCC) is sorafenib (SORA), while HCC has become increasingly drug resistant with enhanced aerobic glycolysis. The present study aimed to examine the chemotherapeutic effects of a flavonoid proanthocyanidin B2 (PB2) on HCC.

METHODS: Five kinds of HCC cell lines and LO2 were used to test the effect of PB2 on aerobic glycolysis. The proliferation, cell cycle, apoptosis and a xenograft mouse model were analyzed. Lentivirus overexpressed pyruvate kinase M2 (PKM2) or sh-PKM2 was used to verify the target of PB2. The detailed mechanism was investigated by immunofluorescence, co-immunoprecipitation, and western blotting.

RESULTS: PB2 inhibited the proliferation, induced cell cycle arrest, and triggered apoptosis of HCC cells in vivo and in vitro. PB2 also suppressed glucose uptake and lactate levels via the direct inhibition of the key glycolytic enzyme, PKM2. In addition, PKM2 inhibited the nuclear translocation of PKM2 and co-localization of PKM2/HIF-1α in the nucleus, leading to the inhibition of aerobic glycolysis. Co-treatment with PB2 was also effective in enhancing the chemosensitivity of SORA.

CONCLUSIONS: PB2 inhibited the expression and nuclear translocation of PKM2, therefore disrupting the interaction between PKM2/HSP90/HIF-1α, to suppress aerobic glycolysis and proliferation, and trigger apoptosis in HCC via HIF-1α-mediated transcription suppression.

Study Type : In Vitro Study

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