MTBP regulates migration and invasion of prostate cancer cells .
10.12122/j.issn.1673-4254.2019.01.02
- Author:
Zhuoyu XIAO
1
;
Mingkun CHEN
1
;
Jiankun YANG
1
;
Cheng YANG
1
;
Xianyuan LÜ
1
;
Hu TIAN
1
;
Cundong LIU
1
Author Information
1. Department of Urology, Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, China.
- Publication Type:Journal Article
- Keywords:
MTBP;
epithelial mesenchymal transition;
invasion;
migration;
prostate cancer
- MeSH:
Antigens, CD;
metabolism;
Cadherins;
metabolism;
Carrier Proteins;
genetics;
metabolism;
Cell Line, Tumor;
Cell Movement;
Epithelial-Mesenchymal Transition;
Gene Expression Regulation, Neoplastic;
Gene Knockdown Techniques;
Humans;
Male;
Neoplasm Invasiveness;
Prostatic Neoplasms;
metabolism;
pathology;
RNA, Small Interfering;
Transfection
- From:
Journal of Southern Medical University
2019;39(1):6-12
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the role of MTBP in regulating the migration and invasion of human prostate cancer cells.
METHODS:The baseline expressions of MTBP in 3 different human prostate cancer cells lines (22RV1, DU145 and Lncap) were detected using Western blotting. The cells were transfected with a small interfering RNA (siRNA) for MTBP knockdown or MTBP plasmid for MTBP overexpression, and 48 h later, the cells were examined for MTBP expression with Western blotting; the changes in the migration abilities of the cells were evaluated using wound healing assay and Transwell assay, and the cell invasiveness was assessed using Matrigel Transwell assay. The expression of E-cadherin protein, a marker of epithelial mesenchymal transition (EMT), was detected using Western blotting.
RESULTS:MTBP expression was the highest in DU145 cells followed by Lncap cells, and was the lowest in 22RV1 cells, indicating a positive correlation of MTBP expression with the level of malignancy of human prostate cancer cells. Transfection of the cells with siRNA or MTBP plasmids efficiently lowered or enhanced the expressions of MTBP in human prostate cancer cells. Wound healing assay showed that inhibition of MTBP expression decreased the migration ability of the prostate cancer cells, and MTBP overexpression significantly promoted the migration of the cells ( < 0.01). Transwell assay showed that MTBP knockdown significantly lowered the migration and invasion ability of the cells, while MTBP overexpression markedly increased the number of migrating and invading cells ( < 0.01); Western blotting results showed that MTBP knockdown increased the expression of E-cadherin protein, and MTBP overexpression decreased E-cadherin expression in the prostate cancer cells.
CONCLUSIONS:MTBP overexpression promotes the migration and invasion of human prostate cancer cells possibly relation to the induction of EMT.
