FCH结构域仅1 (FCHO1)在肺癌中的致癌基因作用

M. Cho, S. Park, Soon‐Kyung Hwang
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引用次数: 0

摘要

Akt或蛋白激酶B是一种丝氨酸/苏氨酸蛋白激酶[4],在磷脂酰肌醇3-激酶(PI3K)下游被多种生长因子激活,包括胰岛素、胰岛素样生长因子- 1和表皮生长因子[5]。活化的Akt (phospho-Akt, p-Akt)是一个强大的细胞存活启动子,因为它可以拮抗和失活凋亡级联的各种成分,如促凋亡Bad、caspase-9和叉头转录因子家族成员[6,7]。PI3K/Akt信号通路通过调节细胞周期蛋白的转录和抑制细胞周期抑制剂来调控G1/S细胞周期转变[8]。细胞周期失调通常与肿瘤发生增加和肿瘤生长加速有关[9]。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Role of FCH Domain Only 1 (FCHO1) as an Oncogene in Lung Cancer
Akt, or protein kinase B, a serine/threonine protein kinase [4], is activated downstream from phosphatidylinositol 3-kinase (PI3K), by various growth factors, including insulin, insulin-like growth factor-I, and epidermal growth factor [5]. Activated Akt (phospho-Akt, p-Akt) is a strong promoter of cell survival because it antagonizes and inactivates various components of the apoptotic cascade such as proapoptotic Bad, caspase-9, and forkhead transcription factor family members [6,7]. The PI3K/Akt signaling pathway regulates the G1/S cell cycle transition by modulating the transcription of cell cycle proteins and suppressing cell cycle inhibitors [8]. A dysregulated cell cycle is often associated with increased tumorigenesis and accelerated tumor growth [9].
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