KIF18B promotes tumor progression through activating the Wnt/β-catenin pathway in cervical cancer
Authors Wu Y, Wang A, Zhu B, Huang J, Lu E, Xu H, Xia W, Dong G, Jiang F, Xu L
Received 18 November 2017
Accepted for publication 3 February 2018
Published 28 March 2018 Volume 2018:11 Pages 1707—1720
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Narasimha Reddy Parine
Peer reviewer comments 2
Editor who approved publication: Dr XuYu Yang
Yaqin Wu,1–3,* Anpeng Wang,1,3,4,* Biqing Zhu,1–3 Jian Huang,2,3 Emei Lu,2,3 Hanzi Xu,2,3 Wenjie Xia,1,3,4 Gaochao Dong,1 Feng Jiang,1,3,4 Lin Xu1,3,4
1Jiangsu Key Laboratory of Molecular and Translational Cancer Research, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, People’s Republic of China; 2Department of Radiation Oncology, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, People’s Republic of China; 3The Fourth Clinical College of Nanjing Medical University, Nanjing, People’s Republic of China; 4Department of Thoracic Surgery, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, People’s Republic of China
*These authors contributed equally to this work
Background: KIF18B was identified as a potential oncogene by analysis of The Cancer Genome Atlas database.
Materials and methods: We assessed KIF18B expression and explored its clinical significance in cervical cancer tissues. We have also evaluated the effects of KIF18B on cervical cancer cell proliferation, migration, and invasion both in vitro and in vivo.
Results: Our results show that KIF18B is overexpressed in cervical cancer tissues and is associated with a large primary tumor size, an advanced FIGO stage, and an advanced tumor grade. Knockdown of KIF18B induces cell cycle G1-phase arrest and inhibits the proliferation, migration, and invasion of cervical cancer cells, whereas its overexpression promotes proliferation, migration, and invasion in these cells. Moreover, silencing of KIF18B reduces expression of CyclinD1, β-catenin, C-myc, and p-GSK3β expression.
Conclusion: These data suggest that KIF18B can serve as a novel oncogene that promotes the tumorigenicity of cervical cancer cells by activating Wnt/β-catenin signaling pathway.
Keywords: KIF18B, cervical cancer, CyclinD1, Wnt/β-catenin signaling pathway
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