Abstract
The chromosomal region 7q was repeatedly found to be rearranged in prostate carcinoma. It harbors several well described candidate tumor suppressor and oncogenes. We addressed two genes with opposite roles in cancer; CAV1, a putative tumor suppressor gene at 7q31, and EZH2 at 7q36, which is believed to promote tumor progression. Our primary aim was to assess their expression changes in primary tumors, and then to elucidate the underlying mechanism, assuming that genomic alterations of either locus could affect the other gene as well. In 35 prostate tumor samples, compared with adjacent tissues, CAV1 was overall downregulated (P < 10-06), whereas EZH2 was significantly overexpressed (P < 10-06). The observed dysregulations were coincident in nearly 70% of the cases. Copy number changes occurred in few tumors. Loss of CAV1 DNA was only marginally associated with reduced expression (P = 0.07), however, and genomic amplification of EZH2 could not explain its upregulation. Through bisulfite sequencing of four tumor samples, CpG-hypermethylation was verified as an alternative mechanism for CAV1 silencing, as reported previously. Moreover, it could also be involved in the reactivation of EZH2.
| Original language | English |
|---|---|
| Journal | Cancer Genetics and Cytogenetics |
| Volume | 182 |
| Issue number | 2 |
| Pages (from-to) | 103-110 |
| Number of pages | 8 |
| ISSN | 0165-4608 |
| DOIs | |
| Publication status | Published - 15.04.2008 |
Funding
We are grateful to Petra Reutter, Margot Brugger, and Antje Kollack for their excellent technical assistance. This work has been supported by the Deutsche Krebshilfe (German Cancer Aid) through grant 70-3111-Vo3 and the National Cancer Institute grant CA 90600-03.
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
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