Over-expressed estrogen receptor-alpha up-regulates hTNF-alpha gene expression and down-regulates beta-catenin signaling activity to induce the apoptosis and inhibit proliferation of LoVo colon cancer cells.

Molecular and Cellular Biochemistry
Hsi-Hsien HsuChih-Yang Huang

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 ERalpha effects on colorectal cancer cells remained un-clear. LoVo cells were transient transfected to overexpress ERalpha, 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 ERalpha 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 ERa...Continue Reading

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Citations

Jul 22, 2008·Medicinal Research Reviews·George G ChenGary Mk Tse
Sep 1, 2008·Clinical and Translational Science·Peng LiScott A Waldman
Jan 23, 2010·Digestive Diseases and Sciences·Dayna S EarlyReina Armamento-Villareal
Dec 4, 2014·World Journal of Gastroenterology : WJG·Hsi-Hsien HsuChih-Yang Huang
Apr 12, 2015·Scandinavian Journal of Gastroenterology·Mariabeatrice PrincipiAlfredo Di Leo
Nov 13, 2008·Annals of Surgical Oncology·Fátima Valdés-MoraJuan Carlos Lacal

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