MicroRNA-361-5p slows down gliomas development through regulating UBR5 to elevate ATMIN protein expression

MicroRNA-361-5p slows down gliomas development through regulating UBR5 to elevate ATMIN protein expression

Blog Article

Abstract 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 pH Test Strips/Labels 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 Heart Dish 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.