Effect of SMYD3 on biological behavior and H3K4 methylation in bladder cancer
Authors Wu X, Xu Q, Chen P, Yu C, Ye L, Huang C, Li T
Received 29 April 2019
Accepted for publication 24 July 2019
Published 2 September 2019 Volume 2019:11 Pages 8125—8133
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Dr Sanjeev Srivastava
Xiang Wu,1,2 Qingjiang Xu,1,2 Pingzhou Chen,1,2 Chenbo Yu,1,2 Liefu Ye,1,2 Chen Huang,1,3 Tao Li1,2
1Shengli Clinical Medical College of Fujian Medical University, Fuzhou 350001, People’s Republic of China; 2Department of Urology, Fujian Provincial Hospital, Fuzhou 350001, People’s Republic of China; 3Department of Thoracic Surgery, Fujian Provincial Hospital, Fuzhou 350001, People’s Republic of China
Correspondence: Tao Li
Department of Urology, Fujian Provincial Hospital, Fuzhou 350001, People’s Republic of China
Tel +86 1 370 507 8075
Purpose: Our goal was to investigate the effect of SMYD3 on the biological behavior and histone 3 lysine-4 (H3K4) methylation of bladder cancer (BLAC).
Patients and methods: qRT-PCR identified that SMYD3 expression level in BLAC cell lines (T24, 5637, BUI-87 and J-82) and human normal uroepithelial cell line SV-HUC1. We also constructed green fluorescence protein lentiviral vector using the gene short hairpin RNA (shRNA) system. We used Western blot to analyze the SMYD3, H3K4me1, H3K4me2 and H3K4me3 expression levels in shRNA transfection lines. We also performed a colony-forming assay to determine colony-forming ability, cell counting kit-8 for cell proliferation detection, Transwell assay to determine cell migration and invasion and Annexin V-FITC/PI double staining to analyze cell apoptosis.
Results: The SMYD3 expression level was significantly higher in BLAC cell lines (T24, 5637, BUI-87 and J-82) than in human normal uroepithelial cell line SV-HUC1, and exhibited the highest expression level in T24 cells, among the cell lines tested. qRT-PCR and Western blot analysis results showed that SMYD3 was successfully suppressed in shRNA transfection lines, and identified that SMYD3 suppression resulted inhibited H3K4me2 and H3K4me3 but not H3K4me1. SMYD3 knockdown cells accelerated cell apoptosis and exhibited low cell colony-forming ability, proliferation ability, inhibition of cell migration and invasion compared with normal cells.
Conclusion: SMYD3 may be activated in BLAC cells to increase H3K4 activity to modulate cell proliferation, migration and invasion ability. The data will be a useful source for future therapy.
Keywords: SMYD3, H3K4 methylation, bladder cancer, cell proliferation
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