ZSCAN10 promotes cell proliferation, upregulates OCT4 expression, and activates Wnt/β-catenin signaling in glioma.

Glioma is the most common malignant brain tumor. The dominant therapeutics including surgery, radiotherapy and chemotherapy do little to improve the survival of patients and the prognosis is disappointing. ZSCAN10 is critical in maintaining the pluripotency of embryonic stem cells. Little information was known about its function in glioma. In this study, ZSCAN10 was shown to be expressed significantly higher in glioma tissues and in cell lines. High ZSCAN10 expression was associated with poor prognosis in glioma. When ZSCAN10 was knocked down, proliferation as well as colony formation of glioma cells were inhibited drastically. In contrast, overexpression of ZSCAN10 promoted cell proliferation and colony formation. However, apoptosis was not affected by ZSCAN10. ZSCAN10 was shown to enhance expression of OCT4 through interaction with the promoter of OCT4 gene by ChIP-qPCR assay and luciferase reporter assay. ZSCAN10 could not promote proliferation of U251 cells when OCT4 was knocked down. In addition, the expression of β-catenin was down-regulated after ZSCAN10 knockdown in U251 cells However, the expression level of DKK1 increased inversely. In summary, ZSCAN10 was associated with survival of glioma patients and contributed to cell proliferation through upregulating OCT4 expression. Moreover, ZSCAN10 might partially participate in the activation of Wnt/β-catenin signaling in glioma. IJCEP