GTSE1 Facilitates the Malignant Phenotype of Lung Cancer Cells via Activating AKT/mTOR Signaling.

Fan Zhang,Hong Jiang,Dongshan Wei,Wen Meng,Xing Feng,Jingfei Meng,Victor H Villar

doi:10.1155/2021/5589532

Abstract

The expression of G2 and S phase-expressed-1 (GTSE1) was upregulated in human cancer. However, its expression and roles in lung cancer have not been identified yet. In our study, we reported that GTSE1 expression was statistically higher in lung tissues than in the adjacent noncancerous tissues which might be a consequence of hypomethylation of the GTSE1 promoter. The upregulated expression of GTSE1 mRNA predicted the poorer survival of the lung patients. Ectopic expression of GTSE1 in lung cancer cells significantly increased while knockdown of GTSE1 decreased cell proliferation, cell migration, and cell invasion in H460 and A549 cells. Furthermore, knockdown of GTSE1 regulated the cell cycle and promoted cell apoptosis in H460 and A549 cells. Finally, we presented that GTSE1 was able to activate AKT/mTOR signaling in H460 and A549 cells. In conclusion, these results indicated that the overexpressed GTSE1 was involved in the progress of lung cancer by promoting proliferation migration and invasion and inhibiting apoptosis of lung cancer cells via activating AKT/mTOR signaling.

Highlights

Lung cancer is one of the most common and deadly cancers worldwide [1, 2]
We reported that the expression of GTSE1 was enhanced in lung cancer tissues and cells, and we think that the hypomethylation of the GTSE1 promoter might be responsible for its high
The proliferation, invasion, and migration of H460 and A549 lung cancer cells were promoted by ectopic expression of GTSE1 while being inhibited by knockdown of GTSE1

Summary

Introduction

Lung cancer is one of the most common and deadly cancers worldwide [1, 2]. Its common molecular function is to bind to the tumor suppressor protein p53 and impede the cancer suppressor ability of p53 in cancers [8]. Some studies further reported that upregulation of GTSE1 was frequently found in several types of human cancers [9, 10]. GTSE1 expression inhibited apoptotic signaling and conferred resistance to cisplatin [12]. The overexpression of GTSE1 suppressed cisplatin sensitivity via p53 apoptotic signaling in gastric cancer [12]. It has been confirmed that the expression of GTSE1was increased in lung cancer, and its high expression has a close relationship to the histological types [13]. The prognosis and roles of GTSE1 have not yet been investigated in the development of lung cancer

Methods

Results

Conclusion