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SET1A-Mediated Mono-Methylation at K342 Regulates YAP Activation by Blocking Its Nuclear Export and Promotes Tumorigenesis.
Fang, Lan; Teng, Hongqi; Wang, Yilin; Liao, Guanghong; Weng, Linjun; Li, Yaxu; Wang, Xinbo; Jin, Jiali; Jiao, Chenchen; Chen, Lei; Peng, Xiaoping; Chen, Jiayu; Yang, Yongzhi; Fang, Houqin; Han, Dongyan; Li, Cheng; Jin, Xueling; Zhang, Shihao; Liu, Zhongchen; Liu, Min; Wei, Qing; Liao, Lujian; Ge, Xin; Zhao, Bin; Zhou, Dawang; Qin, Huan-Long; Zhou, Jun; Wang, Ping.
Afiliação
  • Fang L; Shanghai Tenth People's Hospital of Tongji University, School of Medicine and School of Life Science and Technology, Tongji University, Shanghai 200072, China.
  • Teng H; Shanghai Tenth People's Hospital of Tongji University, School of Medicine and School of Life Science and Technology, Tongji University, Shanghai 200072, China.
  • Wang Y; Department of Hepatic Surgery, Shanghai Cancer Center, Shanghai 200032, China; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
  • Liao G; Shanghai Key Laboratory of Regulatory Biology, East China Normal University, 500 Dongchuan Road, Shanghai 200241, China.
  • Weng L; Shanghai Tenth People's Hospital of Tongji University, School of Medicine and School of Life Science and Technology, Tongji University, Shanghai 200072, China.
  • Li Y; Shanghai Tenth People's Hospital of Tongji University, School of Medicine and School of Life Science and Technology, Tongji University, Shanghai 200072, China.
  • Wang X; Shanghai Tenth People's Hospital of Tongji University, School of Medicine and School of Life Science and Technology, Tongji University, Shanghai 200072, China.
  • Jin J; Shanghai Tenth People's Hospital of Tongji University, School of Medicine and School of Life Science and Technology, Tongji University, Shanghai 200072, China.
  • Jiao C; Shanghai Tenth People's Hospital of Tongji University, School of Medicine and School of Life Science and Technology, Tongji University, Shanghai 200072, China.
  • Chen L; Shanghai Tenth People's Hospital of Tongji University, School of Medicine and School of Life Science and Technology, Tongji University, Shanghai 200072, China.
  • Peng X; Shanghai Tenth People's Hospital of Tongji University, School of Medicine and School of Life Science and Technology, Tongji University, Shanghai 200072, China.
  • Chen J; School of Life Science and Technology, Tongji University, Shanghai 200072, China.
  • Yang Y; Shanghai Tenth People's Hospital of Tongji University, School of Medicine and School of Life Science and Technology, Tongji University, Shanghai 200072, China.
  • Fang H; Shanghai Key Laboratory of Regulatory Biology, East China Normal University, 500 Dongchuan Road, Shanghai 200241, China.
  • Han D; Shanghai Tenth People's Hospital of Tongji University, School of Medicine and School of Life Science and Technology, Tongji University, Shanghai 200072, China.
  • Li C; Shanghai Tenth People's Hospital of Tongji University, School of Medicine and School of Life Science and Technology, Tongji University, Shanghai 200072, China.
  • Jin X; Obstetrics and Gynecology Hospital of Fudan University, Fudan University, Shanghai 200032, China.
  • Zhang S; State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China.
  • Liu Z; Shanghai Tenth People's Hospital of Tongji University, School of Medicine and School of Life Science and Technology, Tongji University, Shanghai 200072, China.
  • Liu M; Institute of Biomedical Sciences, Shandong Provincial Key Laboratory of Animal Resistance Biology, Shandong Collaborative Innovation Center of Cell Biology, College of Life Sciences, Shandong Normal University, Jinan, Shandong 250014, China.
  • Wei Q; Shanghai Tenth People's Hospital of Tongji University, School of Medicine and School of Life Science and Technology, Tongji University, Shanghai 200072, China.
  • Liao L; Shanghai Key Laboratory of Regulatory Biology, East China Normal University, 500 Dongchuan Road, Shanghai 200241, China.
  • Ge X; Shanghai Tenth People's Hospital of Tongji University, School of Medicine and School of Life Science and Technology, Tongji University, Shanghai 200072, China.
  • Zhao B; Life Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Zhejiang 310058, China.
  • Zhou D; State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China.
  • Qin HL; Shanghai Tenth People's Hospital of Tongji University, School of Medicine and School of Life Science and Technology, Tongji University, Shanghai 200072, China.
  • Zhou J; Institute of Biomedical Sciences, Shandong Provincial Key Laboratory of Animal Resistance Biology, Shandong Collaborative Innovation Center of Cell Biology, College of Life Sciences, Shandong Normal University, Jinan, Shandong 250014, China.
  • Wang P; Shanghai Tenth People's Hospital of Tongji University, School of Medicine and School of Life Science and Technology, Tongji University, Shanghai 200072, China. Electronic address: wangp@tongji.edu.cn.
Cancer Cell ; 34(1): 103-118.e9, 2018 07 09.
Article em En | MEDLINE | ID: mdl-30008322
YAP, a key effector of Hippo pathway, is activated by its translocation from cytoplasm to nucleus to regulate gene expression and promote tumorigenesis. Although the mechanism by which YAP is suppressed in cytoplasm has been well-studied, how the activated YAP is sequestered in the nucleus remains unknown. Here, we demonstrate that YAP is a nucleocytoplasmic shuttling protein and its nuclear export is controlled by SET1A-mediated mono-methylation of YAP at K342, which disrupts the binding of YAP to CRM1. YAP mimetic methylation knockin mice are more susceptible to colorectal tumorigenesis. Clinically, YAP K342 methylation is reversely correlated with cancer survival. Collectively, our study identifies SET1A-mediated mono-methylation at K342 as an essential regulatory mechanism for regulating YAP activity and tumorigenesis.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Fosfoproteínas / Neoplasias Colorretais / Núcleo Celular / Transformação Celular Neoplásica / Processamento de Proteína Pós-Traducional / Histona-Lisina N-Metiltransferase / Proteínas Adaptadoras de Transdução de Sinal / Neoplasias Pulmonares Tipo de estudo: Prognostic_studies Limite: Animals / Humans Idioma: En Ano de publicação: 2018 Tipo de documento: Article
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Fosfoproteínas / Neoplasias Colorretais / Núcleo Celular / Transformação Celular Neoplásica / Processamento de Proteína Pós-Traducional / Histona-Lisina N-Metiltransferase / Proteínas Adaptadoras de Transdução de Sinal / Neoplasias Pulmonares Tipo de estudo: Prognostic_studies Limite: Animals / Humans Idioma: En Ano de publicação: 2018 Tipo de documento: Article