WT inhibit human hepatocellular carcinoma BEL-7402 cells growth by modulating Akt and ERK1/2 phosphorylation.
- Author:
Zhang ZHANG
1
;
Chaohui DUAN
;
Kan DING
;
Zhengtao WANG
Author Information
- Publication Type:Journal Article
- MeSH: Blotting, Western; Carcinoma, Hepatocellular; drug therapy; metabolism; Cell Line, Tumor; Drugs, Chinese Herbal; chemistry; therapeutic use; Flow Cytometry; Humans; Liver Neoplasms; drug therapy; metabolism; Mitogen-Activated Protein Kinase 1; metabolism; Mitogen-Activated Protein Kinase 3; metabolism; Molecular Structure; Phosphorylation; drug effects; Proto-Oncogene Proteins c-akt; metabolism; Quinolines; chemistry; therapeutic use
- From: China Journal of Chinese Materia Medica 2009;34(24):3277-3280
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate effects of Akt and ERK1/2 signaling pathways on waltonitone (WT) induced cell growth inhibition in human hepatocellular carcinoma BEL-7402 cells.
METHODCell viability of BEL-7402 cells was examined using MTT assay. Phosphorylation of E Akt and RK1/2 were detected by Western blot analysis, while cell cycle distribution of BEL7402 cells was analyzed by flow cytometry.
RESULTWT could inhibit the BEL-7402 cells growth, induce the S-phase cell cycle arrest, activate Akt and ERK1/2 phosporylation. Moreover, the cell growth inhibition and S-phase cell cycle arrest induction of WT on BEL-7402 cells could be blocked by Akt and ERK1/2 inhibitors.
CONCLUSIONWT induce the cell cycle arrest and inhibit the cell growth on BEL-7402 cells by modulating Akt and ERK1/2 phosphorylation.
