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

• Published in: Life sciences (1973) 2021-07, Vol.276, p.119439-119439, Article 119439
• Main Authors: Wang, Wei, Sun, Ruiying, Zeng, Lizhong, Chen, Yang, Zhang, Na, Cao, Shiguang, Deng, Shanshan, Meng, Xia, Yang, Shuanying
• Format: Article
• Language: English
• Subjects: 1-Phosphatidylinositol 3-kinase; Adenocarcinoma; Adenocarcinoma of Lung - genetics; Adenocarcinoma of Lung - metabolism; Adenocarcinoma of Lung - pathology; Aged; AKT protein; Apoptosis; Biomarkers, Tumor - genetics; Biomarkers, Tumor - metabolism; Biotechnology; Cell migration; Cell Movement; Cell Proliferation; Female; GALNT2; Gene Expression Regulation, Neoplastic; Humans; Immunohistochemistry; Lung adenocarcinoma; Lung Neoplasms - genetics; Lung Neoplasms - metabolism; Lung Neoplasms - pathology; Lungs; Male; Medical prognosis; Metastasis; N-Acetylgalactosaminyltransferases - genetics; N-Acetylgalactosaminyltransferases - metabolism; Neoplasm Invasiveness; Notch; Phenotypes; Phosphatidylinositol 3-Kinases - genetics; Phosphatidylinositol 3-Kinases - metabolism; Polypeptide N-acetylgalactosaminyltransferase; Prognosis; Proliferation; Proto-Oncogene Proteins c-akt - genetics; Proto-Oncogene Proteins c-akt - metabolism; PTEN Phosphohydrolase - genetics; PTEN Phosphohydrolase - metabolism; PTEN protein; Receptor, Notch1 - genetics; Receptor, Notch1 - metabolism; Signal transduction; Signaling; Survival analysis; Survival Rate; Transcription Factor HES-1 - genetics; Transcription Factor HES-1 - metabolism; Tumor Cells, Cultured; Western blotting; Wound healing
• ISSN: 0024-3205; 1879-0631
• DOI: 10.1016/j.lfs.2021.119439

Our study aimed to investigate the function of GALNT2 in lung adenocarcinoma (LUAD). 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. 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. Our data confirmed the cancer-promoting effect of GALNT2, and might provide a new approach for LUAD therapy.