Ninjurin2 overexpression promotes glioma cell growth | Zendy

Li-Na Zhou | Zendy; Ping Li | Zendy; Shang Cai | Zendy; Gang Li | Zendy; Fang Liu | Zendy

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Ninjurin2 overexpression promotes glioma cell growth

Author(s) -

Li-Na Zhou,

Ping Li,

Shang Cai,

Gang Li,

Fang Liu

Publication year - 2019

Publication title -

aging

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.473

H-Index - 90

ISSN - 1945-4589

DOI - 10.18632/aging.102515

Subject(s) - glioma , small hairpin rna , cell growth , protein kinase b , cancer research , ectopic expression , mapk/erk pathway , biology , microbiology and biotechnology , transfection , receptor tyrosine kinase , downregulation and upregulation , chemistry , apoptosis , kinase , cell culture , signal transduction , gene knockdown , gene , biochemistry , genetics

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.

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