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MTSS1 hypermethylation is associated with prostate cancer progression.

Authors :
Chen, Junjie
Huang, Liang
Zhu, Quan
Wang, Zhao
Tang, Zhengyan
Source :
Journal of Cellular Physiology. Mar2020, Vol. 235 Issue 3, p2687-2697. 11p.
Publication Year :
2020

Abstract

This study was conducted to evaluate the influence of DNA methylation of metastasis suppressor 1 (MTSS1) on prostate cancer (PCa) progression. Forty‐nine paired PCa tissue samples and normal tissue samples from The Cancer Genome Atlas were analyzed. Methylome analysis, CpG island arrays and Hierarchical clustering were used to analyze methylation profiles of PCa tissues. MTSS1 methylation level was detected by methylation‐specific PCR. Relative messenger RNA and the expression level of MTSS1 protein were identified by quantitative real‐time PCR (qRT‐PCR) and western blot analysis. The migration, invasion, proliferation, and cell cycle were detected separately by wound‐healing assay, transwell chamber assay, 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl tetrazolium bromide assay and flow cytometry. The roles of MTSS1 in PCa progression were demonstrated in vivo by tumor formation assays in nude mice. MTSS1 expression was decreased in PCa tissues in comparison with paired adjacent normal prostate tissues. Compared to the methylation of MTSS1 in normal prostate tissues based on the MethHC website, the MTSS1 in PCa tissues was hypermethylated. The expression of MTSS1 detected by qRT‐PCR and western blot analysis was found to be downregulated in PCa cells and tissues. The reduced expression of MTSS1 by small interfering RNA‐MTSS1 was recovered by 5‐aza‐2′‐deoxycytidine treatment. Besides, MTSS1 demethylation inhibited migration, invasion, and proliferation of PCa cells, and induced cell cycle to be arrested at G0/G1 phase. Furthermore, it was shown by tumor xenograft assay that MTSS1 inhibited the growth of tumor in vivo. Hypermethylated MTSS1 promoted PCa cells migration, invasion, and proliferation, and suppressed cell cycle arrest at the G0/G1 phase. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
00219541
Volume :
235
Issue :
3
Database :
Academic Search Index
Journal :
Journal of Cellular Physiology
Publication Type :
Academic Journal
Accession number :
140159419
Full Text :
https://doi.org/10.1002/jcp.29172