IndraLab

Statements

USP11 activates FAM126A. 4 / 4
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reach
"25 , 26 , 27 Recently, USP11 was shown to promote HCC development, 28 but the underlying molecular mechanisms involved in this pathogenic process remain poorly understood.In this study, we used a proteomic approach to identify KLF4‐interacting DUBs and firstly discovered that USP11 was responsible for deubiquitinating KLF4 in HCC cells."
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"We also provide mechanistic insights into KLF4 degradation and show that USP11 depletion inhibits growth and chemoresistance of HCC cells by enhancing KLF4 stability."
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"USP11 promotes HCC cell survival, invasion, and metastatic potency in vitro and in vivo."
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"Our functional results provide evidence for the crosstalk between KLF4 and USP11 in hepatic diseases; in particular, they show how USP11 enhances HCC tumorigenesis and steatosis through KLF4 inhibition."
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