肝癌发生中的SGF29和Sry信号通路。
SGF29 and Sry pathway in hepatocarcinogenesis.
作者信息
Kurabe Nobuya, Murakami Shigekazu, Tashiro Fumio
机构信息
Nobuya Kurabe, Department of Tumor Pathology, Hamamatsu University School of Medicine, Shizuoka 431-3192, Japan.
出版信息
World J Biol Chem. 2015 Aug 26;6(3):139-47. doi: 10.4331/wjbc.v6.i3.139.
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.
摘要
c-Myc表达失调是许多人类癌症的一个标志。我们最近发现酵母SPT-ADA-GCN5-乙酰转移酶（SAGA）复合物成分的哺乳动物同源物，即SAGA相关因子29（SGF29）在调节c-Myc过表达中发挥作用。在此，我们讨论了SPT3-TAF9-GCN5-乙酰转移酶复合物（酵母SAGA复合物的对应物）中SFG29的分子特性，以及SGF29表达升高促进肝细胞癌（HCC）中c-Myc致癌潜力的机制。我们提出，性别决定区域Y（Sry）引发的SGF29上游调控在HCC中也会增强。我们假设，由失调的Sry和SGF29途径驱动的c-Myc升高与人类HCC的男性特异性获得有关。
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