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MR Molecular Imaging of Prostate Cancer with a Small Molecular CLT1 Peptide Targeted Contrast Agent
Published on: September 3, 2013
Clusterin (CLU) and prostate cancer.
Federica Rizzi1, Saverio Bettuzzi
1Dipartimento di Medicina Sperimentale, Sezione di Biochimica, Biochimica Clinica e Biochimica dell'Esercizio Fisico, Università di Parma, Via Volturno 39-43100 Parma, Italy.
Advances in Cancer Research
|November 3, 2009
Summary
Clusterin (CLU) expression is downregulated in prostate cancer, contradicting some prior research. Epigenetic silencing via promoter methylation may drive early prostate cell transformation.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- The role of clusterin (CLU) in prostate cancer is controversial, with conflicting reports on its expression levels.
- Some studies suggest CLU promotes prostate cancer, while others indicate it's downregulated during progression.
Purpose of the Study:
- To investigate the role of clusterin (CLU) in prostate tumorigenesis.
- To clarify the contradictory evidence regarding CLU expression in prostate cancer.
Main Methods:
- Meta-analysis of microarray data comparing CLU mRNA in prostate cancer vs. normal tissue.
- Examination of CLU promoter methylation in prostate cancer cell lines (TRAMP-C2, LNCaP).
- Analysis of CLU expression in human prostate carcinomas.
Main Results:
- CLU mRNA was significantly downregulated in prostate cancer tissue across 14 out of 15 studies.
- CLU silencing by promoter methylation was observed in prostate cancer cell lines.
- Reduced CLU expression was found in untreated and hormone-refractory prostate carcinomas.
Conclusions:
- Clusterin (CLU) is downregulated during human prostate cancer progression.
- Epigenetic mechanisms, specifically promoter methylation and chromatin remodeling, play a crucial role in CLU silencing during early prostate cell transformation.
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