1. Academic Validation
  2. FAM60A, increased by Helicobacter pylori, promotes proliferation and suppresses apoptosis of gastric cancer cells by targeting the PI3K/AKT pathway

FAM60A, increased by Helicobacter pylori, promotes proliferation and suppresses apoptosis of gastric cancer cells by targeting the PI3K/AKT pathway

  • Biochem Biophys Res Commun. 2020 Jan 22;521(4):1003-1009. doi: 10.1016/j.bbrc.2019.11.029.
Xinjie Yao 1 Dongyan Liu 2 Linyan Zhou 1 Ying Xie 1 Yan Li 3
Affiliations

Affiliations

  • 1 Department of Gastroenterology, Shengjing Hospital of China Medical University, Shenyang, 110004, Liaoning, China.
  • 2 Medical Research Center, Shengjing Hospital of China Medical University, Benxi, 117000, Liaoning, China.
  • 3 Department of Gastroenterology, Shengjing Hospital of China Medical University, Shenyang, 110004, Liaoning, China. Electronic address: [email protected].
Abstract

Helicobacter pylori (H. pylori) Infection can promote the development of gastric Cancer (GC); however, the underlying mechanism is not clear. FAM60A has been found showing high levels in some Cancer cells, including lung Cancer (A549), and pancreatic Cancer (Capan-2) cell lines. Data in oncomine showed that FAM60A overexpression was an critical prognostic factor in GC. In this study, we showed that knockdown of FAM60A could revert the increase of proliferation and the decrease of Apoptosis caused by H.pylori Infection in HGC-27 and AGS cells. Conversely, FAM60A upregulation promoted proliferation and inhibited Apoptosis in HGC-27 and AGS cells. We also found that the PI3K/Akt pathway inhibitor LY294002 could revert the changes caused by FAM60A upregulation in HGC-27 and AGS cells. Thus, our study provides evidence that FAM60A act as a carcinogen and suggests that H. pylori-induced upregulation of FAM60A may contribute to the development of gastric Cancer.

Keywords

AKT; Cell apoptosis; Cell proliferation; FAM60A; Gastric cancer; H. pylori.

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