The cell effect of Rad23A depletion in mammalian cells

• Main Authors: Chung-Yun Yu, 余中芸
• Other Authors: 莊秀美
• Format: Others
• Language: en_US
• Published: 2013
• Online Access: http://ndltd.ncl.edu.tw/handle/73725805643260919501

碩士 === 國立中興大學 === 生物醫學研究所 === 101 === Rad23 had been identified from yeast with a significant role in 26S proteasome mediated protein degradation. Thus, Rad23 has been reported to involve in many pathways, such as cell cycle regulation, cellular metabolism, and nucleotide excision repair(NER), the most well known function of Rad23. In mammalian cells, there are two isoforms of homologs Rad23A and Rad23B, and they possess the redundant function. However, their individual cell function is not well identified. We use lentiviral RNA interference approach, by hHR23-specific short hairpain RNAs in A549 to establish hHR23 –knockdown cell lines. By this model, we found that knockdown Rad23A resulting in cell morphology alteration and overexpression Rad23A restore cell morphology in A549 cells suggesting that EMT was occurred. In this studies, we demonstrate that hHR23A exerts control over an EMT program that commits sh-HR23A cells to an mesenchymal status highlighted by the expression of N-cadherin, vimentin and down-regulate epithelial markers through regulate protein stability of transcription factor, Twist1.