基因组学与信息重点实验室 

　　例会学术报告 

报告题目：SPOP acts as a key regulatory hub in hypoxia induced kidney tumorigenesis (Published in Cancer Cell)

报告人： 李国强  

主持人： 刘江 研究员

时    间：  2014年4月8日（星期二）上午10:00-11:00

　　地   点：   北京基因组研究所一楼大会议厅 

　　报告摘要： 

　　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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