In Vitro Study on Morusin Regulating Cell Cycle Arrest and Inhibiting Cell Proliferation of ;HCT116 Cells in Colorectal Cancer
10.3969/j.issn.1005-5304.2015.05.020
- VernacularTitle:桑根白皮素调控人结肠癌HCT116细胞周期阻滞及其抑制细胞增殖的体外研究
- Author:
Yuqi ZHOU
;
Min YE
;
Yingcheng ZHANG
;
Pinkang WEI
- Publication Type:Journal Article
- Keywords:
Morusin;
colorectal cancer;
cell cycle;
cell proliferation;
β-catenin pathway
- From:
Chinese Journal of Information on Traditional Chinese Medicine
2015;(5):72-75
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of Morusin on cell line proliferation, cell cycle and cell apoptosis of colorectal cancer HCT116 cell;To discuss its mechanism. Methods HCT116 cells were treated with different concentrations of Morusin for 72 h. Cell proliferation was detected by CCK-8 assay, and cell growth inhibition rate and IC50 value were calculated. HCT116 cells were treated with 25.4, 50.8 μmol/L Morusin for 24 h, 48 h and 72 h. Cell morphology was observed under the microscope, and cell proliferation was detected by CCK-8 assay. After HCT116 cell line was treated with 25.4μmol/L Morusin for 24 h, cell cycle phase distribution was detected by flow cytometry and the cell apoptosis was detected by TUNEL assay under the fluorescence microscope. Post-intervention protein expressions were detected by Western Blot. Results The inhibitory effects of Morusin on the proliferation of HCT116 cell line was concentration/time dependent and IC50 value at 72 h was 25.4μmol/L;Morusin induced the cell cycle arrest at G0/G1 phase and G2/M phase, but there was no induction of cell apoptosis;Morusin significantly decreased the expression ofβ-catenin and its target c-Myc, and downregulated the expressions of cyclinD1 and cyclinB1, which were involved in cell cycle regulation. Conclusion Morusin can inhibit HCT116 cell cycle and the proliferation of colorectal cancer cells. Its mechanism might be realized by suppressing the activity ofβ-catenin pathway and reducing the protein expressions of cyclinD1 and cyclinB1.
