FOXA1 is upregulated in glioma and promotes proliferation as well as cell cycle through regulation of cyclin D1 expression
Authors Zhang C, Yang M, Li Y, Tang S, Sun X
Received 14 March 2018
Accepted for publication 28 April 2018
Published 6 September 2018 Volume 2018:10 Pages 3283—3293
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Professor Harikrishna Nakshatri
Chuanqiang Zhang,1 Meixia Yang,2 Yanmin Li,1 Suwen Tang,1 Xizhou Sun1
1Department of Neurosurgery, Shandong Rizhao City Hospital of Traditional Chinese Medicine, Rizhao, Shandong, 276800, People’s Republic of China; 2Department of Neurology, Shandong Rizhao City Hospital of Traditional Chinese Medicine, Rizhao, Shandong, 276800, People’s Republic of China
Introduction: Forkhead box A1 (FOXA1) has been found to upregulate in numerous cancers, such as ovarian cancer and glioma. However, the detailed function of FOXA1 in glioma is still not known. The purpose of this study was to explore the underlying mechanism of FOXA1 in glioma cell progression.
Methods: The expressions of FOXA1 in glioma tissues and cells were determined using quantitative reverse transcription-polymerase chain reaction and western blotting assays. Wound healing assay and Transwell invasion assay were employed to detect the effects of FOXA1 on cellular migration and invasion. Cell Counting Kit-8 assay, colony formation assay, and flow cytometry analyses were also performed.
Results: Our study results suggested FOXA1 was upregulated in glioma tissues and cells and revealed that FOXA1 promoted glioma cellular proliferation by facilitating G1/S transition. Previous work has indicated that CCND1 expression is regulated by FOXA1 in ovarian cancer. ChIP and qChIP assay as well as dual luciferase reporter assay validated that CCND1 expression was also regulated by FOXA1 in glioma cells. Moreover, over-expression of CCND1 in siFOXA1-transfected cells partly offsets the effect of FOXA1 inhibition on cellular proliferation.
Conclusion: FOXA1 promotes glioma cell progression, including cell proliferation and cell cycle, by targeting CCND1, and shows potential for the development of targeted treatment for glioma.
Keywords: FOXA1, proliferation, invasion, CCND1, glioma
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