Your browser doesn't support javascript.
loading
AMPK Promotes SPOP-Mediated NANOG Degradation to Regulate Prostate Cancer Cell Stemness.
Wang, Xinbo; Jin, Jiali; Wan, Fangning; Zhao, Linlin; Chu, Hongshang; Chen, Cong; Liao, Guanghong; Liu, Jian; Yu, Yue; Teng, Hongqi; Fang, Lan; Jiang, Cong; Pan, Weijuan; Xie, Xin; Li, Jia; Lu, Xiaolin; Jiang, Xuejun; Ge, Xin; Ye, Dingwei; Wang, Ping.
Afiliación
  • Wang X; Tongji University Cancer Center, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai 200072, China; Shanghai Putuo People's Hospital, School of Medicine, Tongji University, Shanghai 200060, China; Institute of Biomedical Sciences and School of Life Sciences, East China
  • Jin J; Tongji University Cancer Center, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai 200072, China; Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai 200241, China.
  • Wan F; Department of Urology, Fudan University Shanghai Cancer Center, Shanghai 200032, China; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
  • Zhao L; Tongji University Cancer Center, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai 200072, China; Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai 200241, China.
  • Chu H; Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai 200241, China.
  • Chen C; Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai 200241, China.
  • Liao G; Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai 200241, China.
  • Liu J; National Center for Drug Screening, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.
  • Yu Y; Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai 200241, China.
  • Teng H; Tongji University Cancer Center, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai 200072, China.
  • Fang L; Tongji University Cancer Center, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai 200072, China.
  • Jiang C; Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai 200241, China.
  • Pan W; Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai 200241, China.
  • Xie X; National Center for Drug Screening, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.
  • Li J; National Center for Drug Screening, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.
  • Lu X; Department of Urology, Fudan University Shanghai Cancer Center, Shanghai 200032, China; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
  • Jiang X; Cell Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.
  • Ge X; Department of Clinical Medicine, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai 200072, China. Electronic address: xin.ge@tongji.edu.cn.
  • Ye D; Department of Urology, Fudan University Shanghai Cancer Center, Shanghai 200032, China; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China. Electronic address: dwyeli@163.com.
  • Wang P; Tongji University Cancer Center, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai 200072, China. Electronic address: wangp@tongji.edu.cn.
Dev Cell ; 48(3): 345-360.e7, 2019 02 11.
Article en En | MEDLINE | ID: mdl-30595535
ABSTRACT
NANOG is an essential transcriptional factor for the maintenance of embryonic stem cells (ESCs) and cancer stem cells (CSCs) in prostate cancer (PCa). However, the regulation mechanism of NANOG protein stability in cancer progression is still elusive. Here, we report that NANOG is degraded by SPOP, a frequently mutated tumor suppressor of PCa. Cancer-associated mutations of SPOP or the mutation of NANOG at S68Y abrogates the SPOP-mediated NANOG degradation, leading to elevated PCa cancer stemness and poor prognosis. In addition, SPOP-mediated NANOG degradation is controlled by the AMPK-BRAF signal axis through the phosphorylation of NANOG at Ser68, which blocked the interaction between SPOP and NANOG. Thus, our study provides a regulation mechanism of PCa stemness controlled by phosphorylation-mediated NANOG stability, which helps to identify novel drug targets and improve therapeutic strategy for PCa.
Asunto(s)
Palabras clave
Texto completo
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Neoplasias de la Próstata / Proteínas Represoras / Proteínas Nucleares / Proteínas Quinasas Activadas por AMP / Proteína Homeótica Nanog Tipo de estudio: Prognostic_studies Límite: Animals / Humans / Male Idioma: En Revista: Dev Cell Asunto de la revista: EMBRIOLOGIA Año: 2019 Tipo del documento: Article
Texto completo
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Neoplasias de la Próstata / Proteínas Represoras / Proteínas Nucleares / Proteínas Quinasas Activadas por AMP / Proteína Homeótica Nanog Tipo de estudio: Prognostic_studies Límite: Animals / Humans / Male Idioma: En Revista: Dev Cell Asunto de la revista: EMBRIOLOGIA Año: 2019 Tipo del documento: Article