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FRA-1 抑制幽门螺杆菌感染的 MGC-803 细胞凋亡。

FRA-1 suppresses apoptosis of Helicobacter pylori infected MGC-803 cells.

机构信息

Clinical Laboratory Center, Jiangsu Taizhou People's Hospital, Taizhou, Jiangsu, People's Republic of China.

School of Medicine, Jiangsu University, Zhenjiang, Jiangsu, People's Republic of China.

出版信息

Mol Biol Rep. 2021 Jan;48(1):611-621. doi: 10.1007/s11033-020-06105-y. Epub 2021 Jan 3.

Abstract

Previous research has demonstrated a correlation between elevated expression of Fos-related antigen 1 (FRA-1) and malignancies. Nevertheless, the role of FRA-1 in Helicobacter pylori infected gastric cancer cells remains vague. Our study aims to investigate whether FRA-1 plays a role in the apoptosis of MGC-803 induced by H. pylori and possible mechanisms. MGC-803 cells were used in vitro to establish a cell model of H. pylori infection. After stimulation with H. pylori, the expression of FRA-1 was increased in MGC-803 cells. H. pylori infection promoted the apoptosis of MGC-803 cells, and led to cell cycle arrest and increased oxidative stress levels. Furthermore, the knockdown of FRA-1 reinforced these changes. H. pylori decreased the expression of Bcl2, Caspase3 and Caspase9, while increased the level of BAX, Cleaved-Caspase3 and Cleaved-Caspase9; in addition, it led to the decrease of major proteins in Ras/Erk and PI3K/AKT signaling pathway. As expected, these changes were augmented by FRA-1 knockdown. Our results demonstrated that high expression of FRA-1 induced by H. pylori suppresses apoptosis in MGC-803 cells which may be regulated by oxidative stress and cycle arrest through caspase family, Ras/Erk and PI3K/AKT signaling pathway.

摘要

先前的研究表明,Fos 相关抗原 1(FRA-1)的高表达与恶性肿瘤之间存在相关性。然而,FRA-1 在幽门螺杆菌感染的胃癌细胞中的作用仍不清楚。本研究旨在探讨 FRA-1 是否在幽门螺杆菌诱导的 MGC-803 细胞凋亡中发挥作用及其可能的机制。我们在体外使用 MGC-803 细胞建立了幽门螺杆菌感染的细胞模型。在受到幽门螺杆菌刺激后,MGC-803 细胞中 FRA-1 的表达增加。幽门螺杆菌感染促进了 MGC-803 细胞的凋亡,并导致细胞周期停滞和氧化应激水平升高。此外,FRA-1 的敲低加强了这些变化。幽门螺杆菌降低了 Bcl2、Caspase3 和 Caspase9 的表达,同时增加了 BAX、Cleaved-Caspase3 和 Cleaved-Caspase9 的水平;此外,它还导致 Ras/Erk 和 PI3K/AKT 信号通路中的主要蛋白减少。正如预期的那样,FRA-1 的敲低增强了这些变化。我们的结果表明,幽门螺杆菌诱导的 FRA-1 高表达抑制了 MGC-803 细胞的凋亡,这可能是通过半胱天冬酶家族、Ras/Erk 和 PI3K/AKT 信号通路调节氧化应激和细胞周期停滞来实现的。

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