FAM60A 被幽门螺杆菌上调后，通过靶向 PI3K/AKT 通路促进胃癌细胞增殖和抑制凋亡。
FAM60A, increased by Helicobacter pylori, promotes proliferation and suppresses apoptosis of gastric cancer cells by targeting the PI3K/AKT pathway.
机构信息
Department of Gastroenterology, Shengjing Hospital of China Medical University, Shenyang, 110004, Liaoning, China.
Medical Research Center, Shengjing Hospital of China Medical University, Benxi, 117000, Liaoning, China.
出版信息
Biochem Biophys Res Commun. 2020 Jan 22;521(4):1003-1009. doi: 10.1016/j.bbrc.2019.11.029. Epub 2019 Nov 12.
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.
幽门螺杆菌（H. pylori）感染可促进胃癌（GC）的发展；然而，其潜在机制尚不清楚。已经发现 FAM60A 在一些癌细胞中高水平表达，包括肺癌（A549）和胰腺癌细胞系（Capan-2）。Oncomine 中的数据显示 FAM60A 过表达是 GC 的一个关键预后因素。在本研究中，我们表明 FAM60A 的敲低可以逆转 H.pylori 感染引起的 HGC-27 和 AGS 细胞增殖增加和凋亡减少。相反，FAM60A 的上调促进了 HGC-27 和 AGS 细胞的增殖并抑制了凋亡。我们还发现，PI3K/AKT 通路抑制剂 LY294002 可以逆转 FAM60A 上调在 HGC-27 和 AGS 细胞中引起的变化。因此，我们的研究提供了证据表明 FAM60A 作为致癌剂发挥作用，并表明 H. pylori 诱导的 FAM60A 上调可能有助于胃癌的发展。
Zotero 插件