Analysis for the roles of MAD1 and LMO7 in regulation of E-cadherin expression

• Main Authors: Jing-chun Huang, 黃景群
• Other Authors: Juang YL
• Format: Others
• Language: zh-TW
• Published: 2011
• Online Access: http://ndltd.ncl.edu.tw/handle/68246874707501757371

碩士 === 慈濟大學 === 微生物學免疫學暨生物化學研究所 === 99 === LIM-domain only 7 (LMO7), a component of adherens junction in epithelial cells, functions as a transcription factor. Previous studies reveal that human LMO7 is a MAD1-interacting protein, and that MAD1 can regulate expression of E-cadherin in MCF-7 breast cancer cells. In this study, we further examined the roles of MAD1 and LMO7 in the expression of E-cadherin. Fluorescence microscopic analysis revealed that MAD1 colocalized with POlR2A within the nucleus. By chromatin immunoprecipitation (ChIP) assay, we confirmed that MAD1 and LMO7 bound to the E-cadherin promoter in MCF7 cancer cells. Since LMO7 is a transcription factor, we further examined the role of LMO7 in expression of E-cadherin. We also performed luciferase assay and western blot analysis to determine expression levels of E-cadherin in different cancer cells when LMO7 was overexpressed or depleted. Our result revealed that overexpression of LMO7 could reduce protein levels of E-cadherin in MCF7 breast cancer cells. Furthermore, overexpression of LMO7 also resulted in a decrease in protein levels of MAD1. In addition, overexpression of LMO7 could cause a dramatic change in morphology of Hela cells. Our observations will be the basis for further investigation of the detailed mechanisms that MAD1 and LMO7 regulate expression of expression of E-cadherin.