Wei Wang1, Ruiying Sun1, Lizhong Zeng1, Yang Chen1, Na Zhang2, Shiguang Cao3, Shanshan Deng1, Xia Meng4, Shuanying Yang5. 1. Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China. 2. Department of Pathology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China. 3. Department of Nuclear Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China. 4. Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China; Department of Pathology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China. Electronic address: mengxiamail@163.com. 5. Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China. Electronic address: yangshuanying66@163.com.
Abstract
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.
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.