Expression changes of CAV1 and EZH2, located on 7q31∼q36, are rarely related to genomic alterations in primary prostate carcinoma

被引：16

作者：

Bachmann, Natascha ^{[1
]}

Haeusler, Juergen ^{[1
]}

Luedeke, Manuel ^{[1
]}

Kuefer, Rainer ^{[2
]}

Perner, Sven ^{[3
]}

Assum, Guenter ^{[1
]}

Paiss, Thomas ^{[2
]}

Hoegel, Josef ^{[1
]}

Vogel, Walther ^{[1
]}

Maier, Christiane ^{[1
]}

机构：

[1] Univ Ulm, Dept Human Genet, D-89081 Ulm, Germany

[2] Univ Ulm, Dept Urol & Ped Urol, D-89081 Ulm, Germany

[3] Univ Ulm, Dept Pathol, D-89081 Ulm, Germany

来源：

CANCER GENETICS AND CYTOGENETICS | 2008年 / 182卷 / 02期

关键词：

D O I：

10.1016/j.cancergencyto.2008.01.006

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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, CAVI 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 CAVI 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 CAVI silencing, as reported previously. Moreover, it could also be involved in the reactivation of EZH2. (C) 2008 Elsevier Inc. All rights reserved.

引用

页码：103 / 110

页数：8

共 42 条

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