Astrocyte elevated gene-1 induces breast cancer proliferation and invasion through upregulating HER2/neu expression.
- Author:
Xin ZHANG
1
;
Ning ZHANG
;
Mei-Xin ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Blotting, Western; Breast Neoplasms; genetics; metabolism; Cell Adhesion Molecules; genetics; metabolism; Cell Line, Tumor; Cell Proliferation; Cell Survival; genetics; physiology; Humans; Neoplasm Invasiveness; genetics; Real-Time Polymerase Chain Reaction; Receptor, ErbB-2; genetics; metabolism; Signal Transduction; genetics; physiology
- From: Chinese Medical Journal 2011;124(21):3546-3550
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDAstrocyte elevated gene-1 (AEG-1), primarily identified as a late response gene induced by HIV-1 infection, plays multiple roles in the process of oncogenesis. This novel gene has been demonstrated to be involved in the several potent carcinogenic pathways, including PI3K/Akt pathway, nuclear factor (NF)-κB pathway, and Wnt/κ-catenin pathway. Although the function of AEG-1 has been intensively investigated in recent years, the molecular mechanism underlying its oncogenic role is largely unknown. The aim of this research was to explore the potential function of AEG-1 in breast cancer development and progression.
METHODSAEG-1 was ectopically overexpressed in breast cancer MCF-7 cells and its biological effects on the proliferation and invasion of MCF-7 cells were studied by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and invasion assays. The expression of HER2/neu, a crucial oncogene involving in breast cancer carcinogenesis, was also determined.
RESULTSOverexpression of the AEG-1 promoted the proliferation and invasion ability of breast cancer cells, and upregulated the expression of HER2/neu, a crucial oncogene involving in breast cancer carcinogenesis.
CONCLUSIONAEG-1 might facilitate the proliferation and invasion of breast cancer cells by upregulating HER2/neu expression, which provides a potential target for breast cancer therapy.