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Laser-capture Microdissection of Human Prostatic Epithelium for RNA Analysis
07:42

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Clusterin is epigenetically regulated in prostate cancer

Hanna E Rauhala1, Kati P Porkka, Outi R Saramäki

  • 1Institute of Medical Technology, University of Tampere, and Tampere University Hospital, Tampere, Finland.

International Journal of Cancer
|July 24, 2008
PubMed

Insights

The TRAMP-C2 mouse model for prostate cancer has few genetic alterations but shows epigenetic silencing of genes, including clusterin. This epigenetic regulation of clusterin is also observed in human prostate cancer.

Area of Science:

  • Oncology
  • Genetics
  • Epigenetics

Background:

  • Prostate cancer research is hindered by a lack of adequate models.
  • The TRAMP mouse model is widely used but not fully characterized for genetic and epigenetic changes.

Purpose of the Study:

  • To screen the TRAMP-C2 cell line for genetic and epigenetic alterations.
  • To compare these alterations with human prostate cancer.
  • To investigate the epigenetic regulation of clusterin in prostate cancer.

Main Methods:

  • Microarray analysis and array comparative genomic hybridization (aCGH) were used to screen for alterations.
  • Demethylation treatment with 5-aza-2'-deoxycytidine followed by expression profiling identified epigenetically silenced genes.
  • Clusterin methylation and expression were analyzed in cell lines and human prostate tumors.

Main Results:

  • TRAMP-C2 cells exhibited limited genomic copy number alterations, but gene copy number and expression were significantly correlated.
  • 43 genes were identified as putatively epigenetically silenced due to promoter hypermethylation.
  • Clusterin was found to be methylated in TRAMP-C2 and LNCaP cells, with significantly reduced expression in human prostate carcinomas.

Conclusions:

  • Epigenetic mechanisms, specifically promoter hypermethylation, play a role in silencing genes in the TRAMP-C2 model.
  • Clusterin is epigenetically regulated in prostate cancer, suggesting its potential involvement in the disease progression.

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