基因組學與信息重點實驗室 

　　例會學術報告 

報告題目：SPOP acts as a key regulatory hub in hypoxia induced kidney tumorigenesis (Published in Cancer Cell)

報告人： 李國強  

主持人： 劉江 研究員

時    間：  2014年4月8日（星期二）上午10:00-11:00

　　地   點：   北京基因組研究所一樓大會議廳 

　　報告摘要： 

　　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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