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MicroRNA-361-5p slows down gliomas development through regulating UBR5 to elevate ATMIN protein expression.
Jia, Jiaoying; Ouyang, Zhu; Wang, Ming; Ma, Wenjia; Liu, Min; Zhang, Mingming; Yu, Mengqiang.
Afiliación
  • Jia J; Department of Neurosurgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
  • Ouyang Z; Department of Neurosurgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
  • Wang M; Department of Neurosurgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
  • Ma W; Department of Neurosurgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
  • Liu M; Department of Neurosurgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
  • Zhang M; Department of Neurosurgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China. zhangmm@csu.edu.cn.
  • Yu M; Department of Neurosurgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China. yumengqiang@csu.edu.cn.
Cell Death Dis ; 12(8): 746, 2021 07 28.
Article en En | MEDLINE | ID: mdl-34321465
MicroRNA (miR)-361-5p has been studied to suppress gliomas development. Based on that, an insight into the regulatory mechanism of miR-361-5p in gliomas was supplemented from ubiquitin protein ligase E3 component N-recognin 5 (UBR5)-mediated ubiquitination of ataxia-telangiectasia mutated interactor (ATMIN). miR-361-5p, ATMIN, and UBR5 levels were clinically analyzed in gliomas tissues, which were further validated in gliomas cell lines. Loss/gain-of-function method was applied to determine the roles of miR-361-5p and UBR5 in gliomas, as to cell viability, migration, invasion, colony formation ability, and apoptosis in vitro and tumorigenesis in vivo. The relationship between miR-361-5p and UBR5 was verified and the interaction between UBR5 and ATMIN was explored. It was detected that reduced miR-361-5p and ATMIN and enhanced UBR5 levels showed in gliomas. Elevating miR-361-5p was repressive in gliomas progression. UBR5 was directly targeted by miR-361-5p. UBR5 can ubiquitinate ATMIN. miR-361-5p suppressed gliomas by regulating UBR5-mediated ubiquitination of ATMIN. Downregulating UBR5 impeded gliomas tumor growth in vivo. Upregulating miR-361-5p targets UBR5 to promote ATMIN protein expression, thus to recline the malignant phenotype of gliomas cells.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Factores de Transcripción / Regulación Neoplásica de la Expresión Génica / MicroARNs / Ubiquitina-Proteína Ligasas / Glioma Límite: Adult / Aged / Animals / Female / Humans / Male / Middle aged Idioma: En Revista: Cell Death Dis Año: 2021 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Factores de Transcripción / Regulación Neoplásica de la Expresión Génica / MicroARNs / Ubiquitina-Proteína Ligasas / Glioma Límite: Adult / Aged / Animals / Female / Humans / Male / Middle aged Idioma: En Revista: Cell Death Dis Año: 2021 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido