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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



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.


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.


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.


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.

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