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SGF29 and Sry pathway in hepatocarcinogenesis.
Kurabe, Nobuya; Murakami, Shigekazu; Tashiro, Fumio.
Afiliação
  • Kurabe N; Nobuya Kurabe, Department of Tumor Pathology, Hamamatsu University School of Medicine, Shizuoka 431-3192, Japan.
  • Murakami S; Nobuya Kurabe, Department of Tumor Pathology, Hamamatsu University School of Medicine, Shizuoka 431-3192, Japan.
  • Tashiro F; Nobuya Kurabe, Department of Tumor Pathology, Hamamatsu University School of Medicine, Shizuoka 431-3192, Japan.
World J Biol Chem ; 6(3): 139-47, 2015 Aug 26.
Article em En | MEDLINE | ID: mdl-26322172
ABSTRACT
Deregulated c-Myc expression is a hallmark of many human cancers. We have recently identified a role of mammalian homolog of yeast SPT-ADA-GCN5-acetyltransferas (SAGA) complex component, SAGA-associated factor 29 (SGF29), in regulating the c-Myc overexpression. Here, we discuss the molecular nature of SFG29 in SPT3-TAF9-GCN5-acetyltransferase complex, a counterpart of yeast SAGA complex, and the mechanism through which the elevated SGF29 expression contribute to oncogenic potential of c-Myc in hepatocellularcarcinoma (HCC). We propose that the upstream regulation of SGF29 elicited by sex-determining region Y (Sry) is also augmented in HCC. We hypothesize that c-Myc elevation driven by the deregulated Sry and SGF29 pathway is implicated in the male specific acquisition of human HCCs.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Prognostic_studies Idioma: En Revista: World J Biol Chem Ano de publicação: 2015 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Prognostic_studies Idioma: En Revista: World J Biol Chem Ano de publicação: 2015 Tipo de documento: Article