Ninjurin2 overexpression promotes glioma cell growth.

Abstract

Ninjurin2 (Ninj2) is an adhesion protein expressed in neurons and glial cells. The current study tested its expression and potential functions in human glioma. We show that Ninj2 mRNA and protein levels are significantly upregulated in human glioma cells and tissues. In established and primary human glioma cells, Ninj2 shRNA or knockout (by CRISPR/Cas9 gene editing) potently inhibited cell survival, growth, proliferation, cell migration and invasion, while inducing apoptosis activation. Contrarily, ectopic overexpression of Ninj2 promoted glioma cell progression in vitro. In human glioma tissues and cells, Ninj2 co-immunoprecipitated with multiple receptor tyrosine kinases (EGFR, PDGFRβ and FGFR), required for downstream Akt and Erk activation. Akt and Erk activation was potently inhibited by Ninj2 shRNA or knockout, but enhanced with ectopic Ninj2 overexpression in glioma cells. In summary, we show that Ninj2 overexpression promotes glioma cell growth.

• Authors: Li-Na Zhou, Ping Li, Shang Cai, Gang Li, Fang Liu
• Journal: Aging (Aging (Albany NY)) Vol. 11 Issue 23 Pg. 11136-11147 (12 02 2019) ISSN: 1945-4589 [Electronic] United States
• PMID: 31794427 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Cell Adhesion Molecules, Neuronal
• NINJ2 protein, human

Topics

• Brain Neoplasms (metabolism, pathology)
• Cell Adhesion Molecules, Neuronal (metabolism)
• Cell Proliferation (physiology)
• Glioma (metabolism, pathology)
• Humans