POU2F2 aggravates cell proliferation and autophagy in lung adenocarcinoma

Abstract

Lung adenocarcinoma (LUAD) is one deadly tumor with high incidence. POU class 2 homeobox 2 (POU2F2) has been notarized to exhibit roles in the regulation of various cancers by playing as a facilitator. Our previous study demonstrated that POU2F2 is highly expressed and accelerates cell proliferation and motility in lung cancer. However, the additional regulatory functions of POU2F2 in LUAD progression require further investigations. In this study, we first confirmed through the UALCAN (A Portal for Facilitating Tumor Subgroup Gene Expression and Survival Analyses) online database that POU2F2 expression is elevated in LUAD tissues. Furthermore, we found that POU2F2 expression is up-regulated in LUAD cell lines. Functional experiments revealed that POU2F2 accelerates LUAD cell proliferation and enhances autophagy through increasing the LC3-II/LC3-I level and fluorescence intensity. Additionally, we discovered that POU2F2 activates the phosphoinositide dependent protein kinase 1 (PDPK1)-mediated phosphatidylinositol-3 kinase (PI3K)/protein kinase B (AKT) pathway. In conclusion, our discovery firstly disclose that POU2F2 exacerbates cell proliferation and autophagy in LUAD by modulating the PI3K/AKT pathway. This work suggests that POU2F2 may be a hopeful bio-marker for treating LUAD.

Keywords

• pou2f2
• lung adenocarcinoma
• autophagy
• pi3k/akt pathway