Literature DB >> 30352438

Overexpression of KIF2A is Suppressed by miR-206 and Associated with Poor Prognosis in Ovarian Cancer.

Nan Sheng, Yun-Zhao Xu, Qing-Hua Xi, Hai-Yan Jiang, Chen-Yi Wang, Yu Zhang, Qing Ye.   

Abstract

BACKGROUND/AIMS: This study aimed to investigate the expression and prognostic value of kinesin family member 2A (KIF2A) and the suppression effects of microRNA-206 (miR-206) on KIF2A in ovarian cancer.
METHODS: Ovarian cancer tissues from patients and ovarian cancer cell lines (A2780 and SKOV3) were used in this study. miR-206 mimics and control were transiently transfected into cells. RT-qPCR was performed to detect KIF2A mRNA and miR-206 expression levels, Western blot was performed to detect KIF2A protein levels, Dual-Luciferase Reporter Assay was used to examine the inhibition effects of miR-206 on KIF2A mRNA, immunohistochemical staining was used to examine the expression of KIF2A in tissue sections. CCK-8, transwell and Annexin-V-FITC/Propidium Iodide staining with flow cytometry were used to detect the cell proliferation, migration/invasion, and apoptosis respectively.
RESULTS: Our study explored the expression profiles of KIF2A and miR-206 in the patients with ovarian cancer. We found that overexpression of KIF2A was associated with a poor prognosis in ovarian cancer. We also found that KIF2A mRNA contains two target sites for miR-206 binding and confirmed that miR-206 directly suppresses KIF2A; inhibits ovarian cancer cell proliferation, migration, and invasion; and induces apoptosis.
CONCLUSION: The results suggest KIF2A could serve a valuable prognostic indicator in ovarian cancer and provide a rationale for treatment of ovarian cancer by targeting KIF2A via miR-206.
© 2018 The Author(s). Published by S. Karger AG, Basel.

Entities:  

Keywords:  Apoptosis; Invasion; KIF2A; Migration; Ovarian Cancer; Proliferation; miR-206

Mesh:

Substances:

Year:  2018        PMID: 30352438     DOI: 10.1159/000494467

Source DB:  PubMed          Journal:  Cell Physiol Biochem        ISSN: 1015-8987


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