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miRNA Expression Analyses in Prostate Cancer Clinical Tissues
11:29

miRNA Expression Analyses in Prostate Cancer Clinical Tissues

Published on: September 8, 2015

Methylation mediated silencing of TMS1/ASC gene in prostate cancer

Partha M Das1, Kavitha Ramachandran, Jane Vanwert

  • 1Sylvester Comprehensive Cancer Center, University of Miami, Miami, FL 33136, USA. pdmanas30@yahoo.com

Molecular Cancer
|July 20, 2006
PubMed
Abstract

Insights

Methylation silences the TMS1/ASC tumor suppressor gene in prostate cancer, offering a potential diagnostic marker. Racial disparities in TMS1/ASC methylation suggest varying prostate cancer susceptibility.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Aberrant promoter methylation silences tumor suppressor genes, contributing to cancer development.
  • The TMS1 (Target of Methylation induced Silencing)/ASC gene, encoding a caspase recruitment domain protein, promotes apoptosis and acts as a tumor suppressor.
  • This study investigates the methylation-induced silencing of the TMS1/ASC gene in prostate cancer.

Purpose of the Study:

  • To investigate the methylation-induced silencing of the TMS1/ASC gene in prostate cancer cell lines.
  • To examine the prevalence of TMS1/ASC gene methylation in prostate cancer tissues.
  • To correlate TMS1/ASC gene methylation with race and clinico-pathological features.

Main Methods:

  • Assessed TMS1/ASC gene expression and promoter methylation in prostate cancer cell lines.
  • Utilized 5-aza-2'deoxycytidine to restore gene expression and Trichostatin A to assess histone deacetylase inhibition.
  • Employed Chromatin Immunoprecipitation (ChIP) assays to analyze protein binding to the TMS1/ASC promoter.
  • Evaluated TMS1/ASC methylation patterns in 66 prostate cancer and 34 benign prostatic hyperplasia tissue samples.

Main Results:

  • Loss of TMS1/ASC gene expression correlated with promoter methylation in LNCaP cells.
  • Demethylating agents restored TMS1/ASC expression, while histone deacetylase inhibitors did not.
  • ChIP assays revealed significant enrichment of MBD3 at the TMS1/ASC promoter.
  • TMS1/ASC methylation was significantly more prevalent in prostate cancer cases among White patients compared to controls (OR 7.6, p=0.002), but not in Black patients (OR 1.1, p=0.91).

Conclusions:

  • Methylation-mediated silencing of TMS1/ASC is a frequent event in prostate cancer, indicating its potential as a diagnostic and prognostic marker.
  • Racial differences in TMS1/ASC methylation patterns highlight the role of molecular markers in prostate cancer susceptibility across ethnic groups.

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