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Knockdown of KIF26B inhibits breast cancer cell proliferation, migration, and invasion

Authors Gu S, Liang H, Qi D, Mao L, Mao G, Qian L, Zhang S

Received 22 January 2018

Accepted for publication 10 April 2018

Published 29 May 2018 Volume 2018:11 Pages 3195—3203


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3

Editor who approved publication: Dr Carlos E Vigil

Shudong Gu,1,* Haibin Liang,2,* Donghui Qi,3 Liyan Mao,4 Guoxin Mao,1 Li Qian,1 Shu Zhang5

1Department of Oncology, Affiliated Hospital of Nantong University, Nantong 226001, China; 2Department of General Surgery, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China; 3Medical College of Nantong University, Nantong 226001, China; 4Department of Endoscopic Diagnosis and Treatment of Digestive Diseases, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China; 5Department of Pathology, Affiliated Hospital of Nantong University, Nantong 226001, China

*These authors contributed equally to this work

Background: Kinesin family member 26B (KIF26B) plays a key role in the development and progression of many human cancers. However, the role and underlying mechanisms of KIF26B in breast cancer cells remain unknown.
Materials and methods: In this study, we inhibited the expression of KIF26B in MDA-MB-231 and MCF-7 cells using lentivirus-delivered shRNA.
Results: Lentivirus-mediated KIF26B knockdown significantly suppressed cell proliferation, colony formation, migration, and invasion. Furthermore, cell cycle analyses revealed that the percentage of cells in the G0/G1 phase was significantly increased in KIF26B knockdown cells. Moreover, the knockdown of KIF26B significantly promoted cell apoptosis via the upregulation of cleaved caspase-3 and Bax.
Conclusion: Our data indicate that KIF26B plays a pivotal role in tumor growth and metastasis in breast cancer cells and may be a potential therapeutic target for treating breast cancer.

Keywords: KIF26B, breast cancer cell, proliferation, migration, invasion

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