作者: Fei Ge , Wenlin Chen , Junying Qin , Zhongmei Zhou , Rong Liu
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摘要: The Kruppel-like factor 5 (KLF5) has been suggested to promote breast cell proliferation, survival and tumorigenesis. KLF5 protein degradation is increased by several E3 ubiquitin ligases, including WWP1 SCFFbw7, through the ubiquitin-proteasome pathway. However, deubiquitinase (DUB) of not demonstrated. In this study, we identified ATXN3L as a DUB genome-wide siRNA screening. directly binds KLF5, decreasing its ubiquitination thus degradation. Functionally, knockdown inhibits cancer proliferation partially KLF5. These findings reveal previously unrecognized role in regulation stability cancer. might be therapeutic target for