Histone methyltransferase SETDB1 is required for prostate cancer cell proliferation, migration and invasion
Open Access
- 1 January 2014
- journal article
- research article
- Published by Medknow in Asian Journal of Andrology
- Vol. 16 (2), 319-324
- https://doi.org/10.4103/1008-682x.122812
Abstract
SETDB1 has been established as an oncogene in a number of human carcinomas. The present study was to evaluate the expression of SETDB1 in prostate cancer (PCa) tissues and cells and to preliminarily investigate the role of SETDB1 in prostate tumorigenesis in vitro. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC) were used to detect the expression of SETDB1 in PCa tissues, adjacent normal tissues, benign prostatic hyperplasia (BPH) tissues, PCa cell lines and normal prostate epithelial cells. The results suggested that SETDB1 was upregulated in human PCa tissues compared with normal tissues at the mRNA and protein levels. The role of SETDB1 in proliferation was analyzed with cell counting kit-8, colony-forming efficiency and flow cytometry assays. The results indicated that downregulation of SETDB1 by siRNA inhibited PCa cell growth, and induced G0/G1 cell cycle arrest. The PCa cell migration and invasion decreased by silcencing SETDB1 which were assessed by using in vitro scratch and transwell invasion assay respectively. Our data suggested that SETDB1 is overexpressed in human PCa. Silencing SETDB1 inhibited PCa cell proliferation, migration and invasion.Keywords
This publication has 31 references indexed in Scilit:
- Epigenetic biomarkers in urological tumors: A systematic reviewCancer Letters, 2014
- Gene amplification of the histone methyltransferase SETDB1 contributes to human lung tumorigenesisOncogene, 2013
- Genome Abnormalities Precede Prostate Cancer and Predict Clinical RelapseThe American Journal of Pathology, 2012
- Polycomb group protein EZH2 is frequently expressed in inflammatory breast cancer and is predictive of worse clinical outcomeCancer, 2011
- A genetic explanation of Slaughter's concept of field cancerization: evidence and clinical implications.2003
- Unsafe SETs: histone lysine methyltransferases and cancerTrends in Biochemical Sciences, 2002
- SETDB1: a novel KAP-1-associated histone H3, lysine 9-specific methyltransferase that contributes to HP1-mediated silencing of euchromatic genes by KRAB zinc-finger proteinsGenes & Development, 2002
- Gene expression analysis of prostate cancersMolecular Carcinogenesis, 2002
- Molecular cloning of ESET, a novel histone H3-specific methyltransferase that interacts with ERG transcription factorOncogene, 2002
- Control of muscle development by dueling HATs and HDACsCurrent Opinion in Genetics & Development, 2001