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Corilagin inhibits hepatocellular carcinoma cell proliferation by inducing G2/ M phase arrest
Author(s) -
Ming Yanlin,
Zheng Zhizhong,
Chen Lianghua,
Zheng Guohua,
Liu Shaosong,
Yu Yinhua,
Tong Qingxuan
Publication year - 2013
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10132
Subject(s) - cyclin dependent kinase 1 , cyclin b1 , cell growth , cell cycle , chemistry , cell cycle checkpoint , flow cytometry , hep g2 , microbiology and biotechnology , pharmacology , in vivo , in vitro , cell , biology , biochemistry
Hepatocellular carcinoma (HCC) is one of most common types of malignant tumours. Therefore, it is very important to identify powerful drugs and their antitumour mechanisms. Corilagin has a significant antitumour potential and lower toxicity in normal cells in vitro. The IC 50 values of corilagin for normal Chang‐liver cells and the HCC cell lines Bel7402 and SMMC7721 were 131.4, 24.5 and 23.4 µM, respectively, in the methyl thiazolyl tetrazolium (MTT) assay. MHCC97‐H xenografts in Balb/c mice intraperitoneally injected with 30 mg/kg corilagin for 5 weeks showed a 47.3% inhibition of tumour growth in vivo. Furthermore, data from flow cytometry and Western blot analyses of cell cycle and cell cycle‐related proteins suggest that corilagin arrests SMMC7721 cells at the G2/M phase by downregulating p‐Akt and cyclin B1/cdc2 and upregulating p‐p53 and p21 Cip1 . In conclusion, corilagin is a potential antitumour drug that is effective in retarding the growth of HCC, which is correlated with the activation of p‐p53‐p21 Cip1 ‐cdc2/cyclin B1.