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Open Access Research article

Bufalin, a component in Chansu, inhibits proliferation and invasion of hepatocellular carcinoma cells

Dong-Ze Qiu1, Zhou-Ji Zhang1, Wei-Zhong Wu2 and Yun-Ke Yang1*

Author Affiliations

1 Department of Traditional Chinese Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, PR China

2 Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Liver Cancer Institute and Zhongshan Hospital, Fudan University, Shanghai 200032, PR China

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BMC Complementary and Alternative Medicine 2013, 13:185  doi:10.1186/1472-6882-13-185

Published: 19 July 2013

Abstract

Background

Hepatocellular carcinoma (HCC) is a common and aggressive cancer, and the treatment options are limited for patients with advanced HCC. Bufalin, the major digoxin-like component of the traditional Chinese medicine Chansu, exhibits significant anti-tumor activities in many tumor cell lines. In the present study, we investigated the effect of bufalin on the inhibition of an AKT-related signaling pathway, and examined the relationship between regulatory proteins and anti-tumor effects in hepatoma cells.

Methods

Proliferation, wound healing, transwell-migration/invasion and adhesion assays were performed in HCCLM3 and HepG2 cell lines. The protein levels of pAKT, AKT, pGSK3β, GSK3β, pβ-catenin, β-catenin, E-cadherin, MMP-9, and MMP-2 were measured by western blot analysis. E-Cadherin and β-catenin expression levels were also evaluated by immunofluorescence.

Results

Bufalin inhibited hepatoma cell proliferation, migration, invasion and adhesion. In addition, treatment with bufalin significantly decreased the levels of pAKT, pGSK3β, MMP-9, and MMP-2, while increasing the levels of GSK3β and E-cadherin and suppressing the nuclear translocation of β-catenin.

Conclusions

Bufalin is a potential anti-HCC therapeutic candidate through its inhibition of the AKT/GSK3β/β-catenin/E-cadherin signaling pathway. Further studies with bufalin are warranted in patients with HCC, especially those with the disease at advanced stages.

Keywords:
Hepatocellular carcinoma; Bufalin; Proliferation; Invasion; AKT signaling pathway