NDLI: Over-expressed estrogen receptor-α up-regulates hTNF-α gene expression and down-regulates β-catenin signaling activity to induce the apoptosis and inhibit proliferation of LoVo colon cancer cells

Content Provider	Springer Nature Link
Author	Hsu, Hsi Hsien Cheng, Sue Fei Chen, Li Mien Liu, Jer Yu Chu, Chun Hsien Weng, Yi Jiun Li, Zih Ying Lin, Chung Sheng Lee, Shin Da Kuo, Wei Wen Huang, Chih Yang
Copyright Year	2006
Abstract	Epidemiologic studies reported that the prevalence of hereditary non-polyposis colon cancer (HNPCC) in male is about 1.5-fold higher than that in female. Decreases in circulatory estrogen (E$_{2}$) have been reported to downregulate the expression of E$_{2}$ receptor (ER) and significantly increase the risk of colorectal cancer. Patients that received E$_{2}$ replacement therapy were found to have a reduction in the incidence of colon adenoma and carcinoma. Furthermore, significant decreases in the expression of ER have been found in colorectal cancer specimens. Evidences strongly suggest the protective roles of E$_{2}$ and ER against colorectal cancer. However, the mechanisms of ERα effects on colorectal cancer cells remained un-clear. LoVo cells were transient transfected to overexpress ERα, DNA fragmentation and the activated caspases measurements were performed to evaluate apoptotic effects. Western blotting was used to evaluate protein levels, and luciferase activity assay to measure the Htnf-a promoter activity. The results clearly demonstrated that overexpressed ERα with or without E$_{2}$ (10$^{−8}$ M) treatment could activate caspase -8, -9, and 3 and induce DNA fragmentation in LoVo cell. At the same time, overexpressed ERα plus E$_{2}$ significantly increases the expression and promoter activity of hTNF-α, and the DNA fragmentation effect induced by E$_{2}$ plus ERα were reduced by the addition of hTNF antibody (0.1 ng(ml). In addition, E$_{2}$ plus ERα significantly upregulated p21 and p27 levels and downregulated the β-catenin and its target genes, cyclin D1 and Rb, which regulate the cell cycle and cell proliferation. The results indicate that E$_{2}$ plus overexpressed ERα induce LoVo cell apoptosis might mediate through the increase of hTNF-α gene expression, which in turn activate caspase-8, -9 and caspase-3 and lead to the DNA fragmentation and apoptosis. E$_{2}$ plus ERα also showed the downregulation of β-catenin signalings implicating the suppression of proliferation and metastasis of colorectal cells. Efforts aiming at enhancing ERα expression and(or activity may be proved to be an alternative therapy against colorectal cancer.
Starting Page	101
Ending Page	109
Page Count	9
File Format	PDF
ISSN	03008177
Journal	Molecular and Cellular Biochemistry
Volume Number	289
Issue Number	1-2
e-ISSN	15734919
Language	English
Publisher	Kluwer Academic Publishers-Plenum Publishers
Publisher Date	2006-04-21
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	LoVo cells E$_{2}$ and estrogen receptor-α tumor necrosis factor-α β-catenin apoptotic effects
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Clinical Biochemistry Molecular Biology

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