Effect of Estradiol-induced E2IG5 on Breast Cancer Cell Line.
- Author:
Jeong Yoon SONG
1
;
Yeon Soo CHANG
;
Suck Hwan KOH
;
Sung Wha HONG
;
Soo Myung OH
;
Choong YOON
;
Yong Koo PARK
;
Jae Hoon PARK
Author Information
1. Singal Kang-Nam Hospital, Korea.
- Publication Type:Original Article
- Keywords:
Breast cancer;
Estradiol;
E2IG5
- MeSH:
Breast Neoplasms*;
Breast*;
Cell Cycle;
Cell Line*;
Cell Proliferation;
Cytochromes c;
Epithelial Cells;
Estradiol;
Estrogens;
Genes, Regulator;
Humans;
Mitochondrial Membranes;
Permeability
- From:Journal of the Korean Surgical Society
2005;68(1):1-8
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Estrogens control the development and cell proliferation of various tissues including the normal mammary epithelial cells, where they induce the expression of the immediate and delayed hormone-responsive genes. The proliferative effects of estrogen have been attributed to its ability to increase the expression of the key cell cycle regulatory genes responsible for cell cycle progression. However, the regulation of cell proliferation is only one aspect of estrogen function. It has also been well documented that estrogen plays a critical role in the etiology and progression of human breast and gynecological cancers. This tumorigenic effect of estrogen might be associated with its anti- apoptotic activities such as of Bcl-2 induction. The aim of this study was to clarify the role of E2IG5, which is an estrogen-induced downstream effector molecule, in breast cancer cell lines. RESULTS: This study shows that E2IG5 is a pro-apoptotic protein that is localized to the mitochondrial membrane via two distinct transmembrane domains. When over-expressed, it induces a mitochondrial permeability transition with the resultant of release cytochrome c and caspase activation. However, three out of four breast cancer cell lines lost their estrogen dependence of E2IG5 expression, which suggests the possible involvement of E2IG5 in the development of breast cancer. CONCLUSION: These results suggest that breast cancer cells may loose their pro-apoptotic signals and selectively use the proliferative mechanism of estrogen, which drives the normal mammary epithelial cells to transform into cancer cells. Further studies using breast cancer tissues will be needed.
