Loading…

Effect of Momordica charantia protein on proliferation, apoptosis and the AKT signal transduction pathway in the human endometrial carcinoma Ishikawa H cell line in vitro

Endometrial carcinoma (EC) is one of the most common female malignancies, and there is an urgent requirement to explore new therapeutic strategies. In the present study, Ishikawa H cells were treated with protein (MCP30). The cell morphology, growth inhibition rate, cell cycle distribution, and expr...

Full description

Saved in:
Bibliographic Details
Published in:Oncology letters 2017-05, Vol.13 (5), p.3032-3038
Main Authors: Gu, Hang-Zhi, Lin, Rong-Rong, Wang, Han-Chu, Zhu, Xue-Jie, Hu, Yan, Zheng, Fei-Yun
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Endometrial carcinoma (EC) is one of the most common female malignancies, and there is an urgent requirement to explore new therapeutic strategies. In the present study, Ishikawa H cells were treated with protein (MCP30). The cell morphology, growth inhibition rate, cell cycle distribution, and expression of phosphate and tensin homolog, P-AKT and AKT were measured. DNA fragmentation analysis and Annexin V-fluorescein isothiocyanate/propidium iodide double staining assay were used to analyze cell apoptosis. MCP30 decreased the viability of Ishikawa H cells in a dose- and time-dependent manner. The early apoptotic rates of Ishikawa H cells treated with MCP30 at 666.67 pM reached to 16.07±0.15%, following 72 h of treatment. DNA ladder was observed in cells treated with 333.33 and 666.67 pM MCP30 following 72 h of treatment. MCP30 blocks Ishikawa H cells from progressing between the S-phase and the G2/M-phase in a time- and concentration-dependent manner. Western blotting revealed that MCP30 treatment decreased the levels of P-AKT in a dose-dependent manner. It was revealed that MCP30 decreases cell proliferation, and induces apoptosis and S-phase cell cycle arrest through the AKT signaling pathway in Ishikawa H cells.
ISSN:1792-1074
1792-1082
DOI:10.3892/ol.2017.5830