Promotes Cell Growth and Resistance to Temozolomide Through Regulating Notch Signal Pathway in Glioma.

BACKGROUND

Glioma is a fatal primary malignant tumor. We aimed to explore the effect of nuclear receptor subfamily 5 group A member 2 () on glioma.

METHODS

expression in glioma tissues and cells was detected using qRT-PCR and immunohistochemistry (IHC)/Western blot. SPSS 22.0 was performed to explore the relationship between expression and glioma clinicopathologic features. The down-expressed plasmid of was transfected into glioma cells, and the cell viability, proliferation, apoptosis, migration, and invasion were respectively determined by MTT, EdU, flow cytometry, wound healing and transwell assays. Cell cycle was analyzed using flow cytometry. Temozolomide (TMZ)-resistant glioma cells were established to define the effect of on drug resistance. The expressions of Notch pathway-related proteins were assessed by Western blot. Glioma nude mice model was constructed to explore the role of played in vivo.

RESULTS

was highly expressed in glioma tissues and cell lines. overexpression was related to the poor prognosis of glioma patients. knockdown inhibited cell viability, proliferation, migration, and invasion, induced cell cycle arrest and promoted cell apoptosis in U138 and U251 cells. In U138/TMZ and U251/TMZ cell lines, upregulation enhanced TMZ resistance while downregulation reduced it. The knockdown of influenced the expressions of Notch pathway-related proteins. knockdown suppressed tumor growth and facilitated apoptosis in glioma mice model.

CONCLUSION

affected glioma cell malignant behaviors and TMZ resistance via Notch signaling pathway and it might be a novel target in glioma therapy.