Abstract
Prostate cancer (CaP) is the most common malignant tumor diagnosed in men worldwide. Although the pathogenesis of CaP at the molecular level is not exactly mapped as the pathogenesis of colorectal cancer, our knowledge in this field has been largely increased in recent years.
In addition to genetic changes, epigenetic changes can also contribute to the initiation and progression of this disease. There are three types of epigenetic changes currently intensively investigated: DNA methylation, chromatin remodeling and regulation of gene expression by microRNA molecules (miRNAs).
The current model of the pathogenesis of CaP is based on the sequential accumulation of changes in the prostate tissue, including loss of gene expression of HPC1, changes in the gene for the androgen receptor (AR) and others. The course of the disease is strongly influenced by the presence of fusion gene TMPRSS2-ETS in PIN lesions and the switch to androgen-independent tumor growth.
Deregulation of expression of miR-20a, miR-21, miR-25, miR-34a and miR-205 in prostate cancer affects the activation of apoptosis and inhibition proapoptotic signals. In addition to inhibition of apoptosis, proliferation control deregulation is essential for cancer cells.
Overexpression of miR-221/222 and a suppression of miR-15a/16-1 expression support process of proliferation in CaP. With the increase in understanding of miRNA molecules involved in the pathogenesis of CaP, their use as biomarkers and as targets for anticancer therapy is expected.
Hopefully some of these molecules will be also used in diagnostics of CaP as new tumor markers such as TMPRSS2-ETS and PCA3/DD3.