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Article Publish Status: FREE
Abstract Title:

Ginsenoside Rh2 inhibits hepatocellular carcinoma throughβ-catenin and autophagy.

Abstract Source:

Sci Rep. 2016 Jan 19 ;6:19383. Epub 2016 Jan 19. PMID: 26783250

Abstract Author(s):

Zhiqing Yang, Tingting Zhao, Hongli Liu, Leida Zhang

Article Affiliation:

Zhiqing Yang

Abstract:

Hepatocellular carcinoma (HCC) is the most common liver cancer, with a very poor prognosis. There is an urgent need for an effective therapy for HCC. Ginsenoside Rh2 (GRh2) has been shown to significantly inhibit growth of some types of cancer, whereas its effects on HCC have not been examined. Here, we treated human HCC cells with different doses of GRh2, and found that GRh2 dose-dependently reduced HCC viability, in either CCK-8 assay or MTT assay. The effects of GRh2 on the cancer stem cells (CSCs)-like cells were determined by aldefluor flow cytometry and by tumor sphere formation, showing that GRh2 dose-dependently decreased the number of these CSCs-like cells in HCC. Autophagy-associated protein andβ-catenin level were measured in GRh2-treated HCC cells by Western blot, showing that GRh2 increased autophagy and inhibited β-catenin signaling. Expression of short hairpin small interfering RNA (shRNA) for Atg7 in HCC cells completely abolished the effects of GRh2 on β-catenin and cell viability, while overexpression of β-catenin abolished the effects of GRh2 on autophagy and cell viability. Together, our data suggest that GRh2 may inhibit HCC cell growth, possibly through a coordinated autophagy and β-catenin signaling.

Study Type : In Vitro Study

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