GALNT2 promotes cell proliferation, migration, and invasion by activating the Notch/Hes1-PTEN-PI3K/Akt signaling pathway in lung adenocarcinoma

Aims: Our study aimed to investigate the function of GALNT2 in lung adenocarcinoma (LUAD). Main methods: We used network tools and tissue microarray immunohistochemistry to measure the expression levels of GALNT2 in LUAD. Kaplan-Meier curves and Cox regression methods were used in survival analysis. We detected the role of GALNT2 in cell lines by Cell Counting Kit-8, colony formation, transwell, and wound healing assays. We performed Western blotting to evaluate downstream protein levels. Key findings: GALNT2 was highly expressed in LUAD samples and indicated a poor prognosis. Knockdown of GALNT2 suppressed cell line proliferation, migration, and invasion abilities, while overexpression of GALNT2 enhanced those phenotypes. Moreover, GALNT2 activated Notch/Hes1-PTEN-PI3K/Akt signaling axis. Significance: Our data confirmed the cancer-promoting effect of GALNT2, and might provide a new approach for LUAD therapy.

Automated summary

The study revealed that GALNT2 is highly expressed in LUAD and is associated with poor prognosis. GALNT2 promotes cancer cell proliferation and migration by activating the Notch/Hes1-PTEN-PI3K/Akt signaling axis, suggesting a potential new therapeutic target for LUAD.