AKT plays a crucial role in gastric cancer

Abstract

The AKT protein is involved in the phosphatidylinositol-3 kinase signaling pathway and is a vital regulator of survival, proliferation and differentiation in various types of cells. Helicobacter pylori infection induces epithelial cell proliferation and oxidative stress in chronic gastritis. These alterations lead to telomere shortening, resulting in the activation of telomerase. AKT, in particular, is activated by H. pylori-induced inflammation. AKT then promotes the expression of human telomerase reverse transcriptase, which encodes a catalytic subunit of telomerase, and induces telomerase activity, an essential component of the process of carcinogenesis. AKT activation is increased in gastric mucosa with carcinogenic properties and is associated with the low survival of patients with gastric cancer. The findings of the present study suggest that AKT is pivotal in gastric carcinogenesis and progression.

Keywords: Helicobacter pylori; chronic gastritis; hTERT; telomerase.

Figure 1.

Central role of AKT in H. pylori-induced gastric carcinogenesis. hTERT, human telomerase reverse transcriptase; ROS, reactive oxide species; iNOS, inducible nitric oxide synthase; PI3K, phosphatidylinositol-3 kinase; H. pylori, Helicobacter pylori.