Molecular mechanism of proliferation of human breast cancer cell MCF-7 inhibited by E1A gene.
- Author:
Jia CHEN
1
;
Liang-Fang SHEN
;
Mei-Zuo ZHONG
Author Information
1. Department of Oncology, Xiangya Hospital, Central South University, Changsha 410008, China.
- Publication Type:Journal Article
- MeSH:
Adenovirus E1A Proteins;
biosynthesis;
genetics;
Apoptosis;
genetics;
Breast Neoplasms;
genetics;
metabolism;
Cell Proliferation;
Female;
Genes, erbB-2;
genetics;
Humans;
RNA, Messenger;
biosynthesis;
genetics;
Receptor, ErbB-2;
biosynthesis;
genetics;
Transfection;
Tumor Cells, Cultured
- From:
Journal of Central South University(Medical Sciences)
2008;33(7):582-586
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To explore the molecular mechanism of proliferation inhibition of human breast cancer cell MCF-7 regulated by E1A gene.
METHODS:E1A gene was transfected into MCF-7 cells by liposome reagents. RT-PCR and Western blot were used to detect E1A mRNA and protein expression and HER-2 mRNA in MCF-7. The proliferation and colony formation of MCF-7 were measured by 3-(4,5-dinmethylthiahiazo-z-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and soft agar formation assay. The apoptosis of MCF-7 cells regulated by E1A expression was examined by flow cytometry.
RESULTS:E1A was not endogenously expressed in MCF-7. E1A expression in MCF-7 could significantly decrease HER-2 mRNA and protein expression. Flow cytometry indicated that the apoptosis of MCF-7 could be induced by E1A. Meanwhile, E1A gene could significantly inhibit MCF-7 proliferation and colony formation in soft agar.
CONCLUSION:E1A gene can decrease HER-2 expression and induce the apoptosis of human breast cancer cell MCF-7, and inhibit the proliferation and colony formation of MCF-7.
