【摘 要】
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Large tumor suppressor 1 (LATS1) is the key kinase controlling activation of Hippo signalling pathway.Post-translational modifications of LATS 1 modulate its kinase activity.However,detailed mechanism underlying LATS 1 stability and activation remains elu
【机 构】
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Department of Human Anatomy,Histology and Embryology,MOE Key Laboratory of Carcinogenesis and Transl
论文部分内容阅读
Large tumor suppressor 1 (LATS1) is the key kinase controlling activation of Hippo signalling pathway.Post-translational modifications of LATS 1 modulate its kinase activity.However,detailed mechanism underlying LATS 1 stability and activation remains elusive.Here we report that LATS1 is acetylated by acetyltransferase CBP at K751 and is deacetylated by deacetylases SIRT3 and SIRT4.Acetylation at K751 stabilized LATS1 by decreasing LATS1 ubiquitination and inhibited LATS1 activation by reducing its phosphorylation.Mechanistically,LATS1 acetylation resulted in inhibition of YAP phosphorylation and de-gradation,leading to increased YAP nucleus translocation and promoted target gene expression.Functionally,LATS1-K751Q,the acetylation mimic mutant potentiated lung cancer cell migration,invasion and tumor growth,whereas LATS1-K751R,the acetylation deficient mutant inhibited these functions.Taken together,we demonstrated a previously unidentified post-trans-lational modification of LATS 1 that converts LATS 1 from a tumor suppressor to a tumor promoter by suppression of Hippo signalling through acetylation of LATS 1.
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