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.
Highlights
Glioma is a common brain malignancy, causing significant mortalities each year [1,2,3]
Ninj2 is upregulated in human glioma cells and tissues
MRNA levels were significantly elevated in established human glioma cell lines (A172 and U251MG) and primary human glioma cells (Figure 1A)
Summary
Glioma is a common brain malignancy, causing significant mortalities each year [1,2,3]. High-grade (grade III-IV) gliomas (i.e. glioblastoma) have one worse prognosis among all human malignancies [1,2,3]. The molecular heterogeneity are commonly detected in human gliomas [1], leading to dysregulation and overactivation of multiple signaling cascades [7,8,9]. These cascades, including PI3K-Akt-mTOR and ErkMAPK signaling, shall promote glioma tumorigenesis and progression [7,8,9]. The molecularly targeted therapy has become the research focus for glioma therapies [7,8,9,10,11]
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