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

  • Wei Wang
  • , Ruiying Sun
  • , Lizhong Zeng
  • , Yang Chen
  • , Na Zhang
  • , Shiguang Cao
  • , Shanshan Deng
  • , Xia Meng
  • , Shuanying Yang

Research output: Contribution to journalArticlepeer-review

30 Scopus citations

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.

Original languageEnglish
Article number119439
JournalLife Sciences
Volume276
DOIs
StatePublished - 1 Jul 2021
Externally publishedYes

Keywords

  • GALNT2
  • Lung adenocarcinoma
  • Metastasis
  • Notch
  • Proliferation

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