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The Glucose-Regulated MiR-483-3p Influences Key Signaling Pathways in Cancer.
Pepe, Felice; Visone, Rosa; Veronese, Angelo.
Afiliação
  • Pepe F; Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210, USA. Felice.Pepe@osumc.edu.
  • Visone R; Ageing Research Center and Translational Medicine-CeSI-MeT, 66100 Chieti, Italy. r.visone@unich.it.
  • Veronese A; Department of Medical, Oral and Biotechnological Sciences, G. d'Annunzio University Chieti-Pescara, 66100 Chieti, Italy. r.visone@unich.it.
Cancers (Basel) ; 10(6)2018 Jun 04.
Article em En | MEDLINE | ID: mdl-29867024
The hsa-mir-483 gene, located within the IGF2 locus, transcribes for two mature microRNAs, miR-483-5p and miR-483-3p. This gene, whose regulation is mediated by the the CTNNB1/USF1 complex, shows an independent expression from its host gene IGF2. The miR-483-3p affects the Wnt/ß-catenin, the TGF-ß, and the TP53 signaling pathways by targeting several genes as CTNNB1, SMAD4, IGF1, and BBC3. Accordingly, miR-483-3p is associated with various tissues specific physiological properties as insulin and melanin production, as well as with cellular physiological functions such as wounding, differentiation, proliferation, and survival. Deregulation of miR-483-3p is observed in different types of cancer, and its overexpression can inhibit the pro-apoptotic pathway induced by the TP53 target effectors. As a result, the oncogenic characteristics of miR-483-3p are linked to the effect of some of the most relevant cancer-related genes, TP53 and CTNNB1, as well as to one of the most important cancer hallmark: the aberrant glucose metabolism of tumor cells. In this review, we summarize the recent findings regarding the miR-483-3p, to elucidate its functional role in physiological and pathological contexts, focusing overall on its involvement in cancer and in the TP53 pathway.
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Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2018 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2018 Tipo de documento: Article