AURKB Promotes the Metastasis of Gastric Cancer, Possibly by Inducing EMT
Authors Wang Z, Yu Z, Wang G, Zhou Y, Deng J, Feng Y, Chen J, Tian L
Received 17 March 2020
Accepted for publication 9 July 2020
Published 5 August 2020 Volume 2020:12 Pages 6947—6958
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Ahmet Emre Eskazan
Zhen Wang ,* Zhu Yu ,* Gong-he Wang, Yi-ming Zhou, Jian-ping Deng, Yue Feng, Jun-qiang Chen, Lei Tian
Department of Gastrointestinal Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Lei Tian; Jun-qiang Chen Email firstname.lastname@example.org; email@example.com
Aim: To investigate the function of Aurora kinase B (AURKB) in gastric cancer (GC).
Methods: Immunohistochemistry was used to assay the expression of AURKB in 50 pairs of GC and adjacent tissues, and qRT-PCR was conducted to test AURKB expression in normal gastric epithelial and GC cell lines. Two segments of small interference RNAs (siRNAs) targeting AURKB were synthesized and inserted into GV248 lentivirus vector. After transfected with LV-AURKB-RNAis, CCK8, wound healing, transwell and flow cytometric assays were performed to determine the influence of silencing AURKB on cell proliferation, invasion, migration, cell cycles and apoptosis of GC cells, and the expression of EMT (epithelial–mesenchymal transition)-related markers was demonstrated by Western blots (WB).
Results: AURKB was highly expressed in GC and closely associated with lymph node metastasis and advanced stages of GC. Down-regulating AURKB suppressed the proliferation and promoted the apoptosis of GC cells, arrested the cell cycle in G2/M phase, and inhibited the invasion and migration of GC cells. The expression levels of AKT1, mTOR, Myc, MMP2, and VEGFA were decreased, while the expression levels of OCLN and JUP were increased after knocking down of AURKB in both AGC and MKN45 cells.
Conclusion: AURKB is overexpressed in GC and closely associated with clinicopathologic characteristics of GC. It is likely that by inhibiting VEGFA/Akt/mTOR and Wnt/β-catenin/Myc pathways, silenced AURKB could inhibit the invasive and migratory abilities of GC cells. However, because of the small sample size and the absence of in-vivo experiments, these results should be verified by further studies.
Keywords: AURKB, gastric cancer, metastasis, EMT
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