Institute of Traumatic Brain Injury and Neurology of the Chinese Peoples Armed Police Forces

Tianjin, China

Institute of Traumatic Brain Injury and Neurology of the Chinese Peoples Armed Police Forces

Tianjin, China
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Sun H.-T.,Institute of Traumatic Brain Injury and Neurology of the Chinese Peoples Armed Police Forces | Cheng S.-X.,Institute of Traumatic Brain Injury and Neurology of the Chinese Peoples Armed Police Forces | Tu Y.,Institute of Traumatic Brain Injury and Neurology of the Chinese Peoples Armed Police Forces | Li X.-H.,Institute of Traumatic Brain Injury and Neurology of the Chinese Peoples Armed Police Forces | Zhang S.,Institute of Traumatic Brain Injury and Neurology of the Chinese Peoples Armed Police Forces
PLoS ONE | Year: 2013

Background: Forkhead box Q1 (FoxQ1) is a member of the forkhead transcription factor family, and it has recently been found to participate in cancer development. However, whether FoxQ1 expression contributes to glioma development and progression is not known. We investigate FoxQ1 expression in gliomas and the role of FoxQ1 during tumorgenesis. Methods: Reverse transcription quantitative real-time PCR (RT-qPCR) and Western blot were used to determine the FoxQ1 and Neurexins 3 (NRXN3) expression in gliomas. Chromatin immunoprecipitation (ChIP) and luciferase assays were used to determine the regulation between FoxQ1 and NRXN3. We established depleted FoxQ1 stable clones in U-87MG cells and overexpressed FoxQ1 stable clones in SW1088 cells. MTT and transwell were used to evaluate the ability of proliferation and migration, respectively. Results: FoxQ1 mRNA and protein were up-regulated in gliomas and negatively related to the NRXN3 expression (r = -0.373, P = 0.042). FoxQ1 directly binds to NRXN3 promoter region and suppresses the promoter activity. Furthermore, the ability of proliferation and migration is reduced in depleted FoxQ1 cells. Conclusion: FoxQ1 promotes glioma cell proliferation and migration by down-regulation of NRXN3 expression. © 2013 Sun et al.

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