title: Corilagin inhibits hepatocellular carcinoma cell proliferation by inducing G2/M phase arrest.
abstract: 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 IC50 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.
authors.affiliation: The Research and Development Center for Medicinal Plants and Plant Drugs, Xiamen Overseas Chinese Subtropical Plant Introduction Garden, Gusheng Road 4#, Xiamen, 361002, Fujian Province, China. xmyanlin@gmail.com
authors.forename: Yanlin
authors.initials: Y
authors.lastname: Ming
authors.forename: Zhizhong
authors.initials: Z
authors.lastname: Zheng
authors.forename: Lianghua
authors.initials: L
authors.lastname: Chen
authors.forename: Guohua
authors.initials: G
authors.lastname: Zheng
authors.forename: Shaosong
authors.initials: S
authors.lastname: Liu
authors.forename: Yinhua
authors.initials: Y
authors.lastname: Yu
authors.forename: Qingxuan
authors.initials: Q
authors.lastname: Tong
mesh_terms: D000818:Animals; D016203:CDC2 Protein Kinase / Q000378:metabolism; D006528:Carcinoma, Hepatocellular / Q000378:metabolism / Q000473:pathology*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D048430:Cell Shape / Q000187:drug effects; D002945:Cisplatin / Q000494:pharmacology; D056744:Cyclin B1 / Q000378:metabolism; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000378:metabolism; D059565:G2 Phase Cell Cycle Checkpoints / Q000187:drug effects*; D005960:Glucosides / Q000737:chemistry / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D047348:Hydrolyzable Tannins; D008113:Liver Neoplasms / Q000378:metabolism / Q000473:pathology*; D059566:M Phase Cell Cycle Checkpoints / Q000187:drug effects*; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D008954:Models, Biological; D015398:Signal Transduction / Q000187:drug effects; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D023041:Xenograft Model Antitumor Assays
chemical_list: D056744:Cyclin B1; D050759:Cyclin-Dependent Kinase Inhibitor p21; D005960:Glucosides; D047348:Hydrolyzable Tannins; D016159:Tumor Suppressor Protein p53; C049096:corilagin; D016203:CDC2 Protein Kinase; D002945:Cisplatin
keywords: antitumour; corilagin; hepatocellular carcinoma; molecular mechanisms; signalling pathway