基因组学与信息重点尝试室 

　　例会学术汇报 

汇报标题：SPOP acts as a key regulatory hub in hypoxia induced kidney tumorigenesis (Published in Cancer Cell)

年报Journal

汇报人： 李国强  

主持人： 刘江 钻研员

时    间：  2014年4月8日（星期二）上午10:00-11:00

　　地   点：   北京基因组钻研所一楼大会议厅 

　　汇报提要： 

　　Hypoxic stress and hypoxia-inducible factors (HIFs) play important roles in a wide range of tumors. We demonstrate that SPOP, which encodes an E3 ubiquitin ligase component, is a direct transcriptional target of HIFs in clear cell renal cell carcinoma (ccRCC). Furthermore, hypoxia results in cytoplasmic accumulation of SPOP, which is sufficient to induce tumorigenesis. This tumorigenic activity occurs through the ubiquitination and degradation of multiple regulators of cellular proliferation and apoptosis, including the tumor suppressor PTEN, ERK phosphatases, the proapoptotic molecule Daxx, and the Hedgehog pathway transcription factor Gli2. Knockdown of SPOP specifically kills ccRCC cells, indicating that it may be a promising therapeutic target. Collectively, our results indicate that SPOP serves as a regulatory hub to promote ccRCC tumorigenesis. 

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