SGF29和Sry通路在肝癌发生中的作用。

Nobuya Kurabe, Shigekazu Murakami, Fumio Tashiro
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引用次数: 9

摘要

失控的c-Myc表达是许多人类癌症的标志。我们最近发现了酵母spt - ada - gcn5 -乙酰转移蛋白(SAGA)复合物组分的哺乳动物同源物,SAGA相关因子29 (SGF29)在调节c-Myc过表达中的作用。在这里,我们讨论了SGF29在spt3 - taf9 - gcn5 -乙酰转移酶复合体(酵母SAGA复合体的对应物)中的分子性质,以及SGF29表达升高导致c-Myc在肝细胞癌(HCC)中致癌的机制。我们提出,由性别决定区Y (Sry)引发的SGF29的上游调控在HCC中也得到增强。我们假设由失调的Sry和SGF29通路驱动的c-Myc升高与人类hcc的男性特异性获得有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

SGF29 and Sry pathway in hepatocarcinogenesis.

SGF29 and Sry pathway in hepatocarcinogenesis.

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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