TY - JOUR
T1 - Expression changes of CAV1 and EZH2, located on 7q31∼q36, are rarely related to genomic alterations in primary prostate carcinoma
AU - Bachmann, Natascha
AU - Haeusler, Juergen
AU - Luedeke, Manuel
AU - Kuefer, Rainer
AU - Perner, Sven
AU - Assum, Guenter
AU - Paiss, Thomas
AU - Hoegel, Josef
AU - Vogel, Walther
AU - Maier, Christiane
N1 - Funding Information:
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.
Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2008/4/15
Y1 - 2008/4/15
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=41749119194&partnerID=8YFLogxK
U2 - 10.1016/j.cancergencyto.2008.01.006
DO - 10.1016/j.cancergencyto.2008.01.006
M3 - Journal articles
C2 - 18406871
AN - SCOPUS:41749119194
SN - 0165-4608
VL - 182
SP - 103
EP - 110
JO - Cancer Genetics and Cytogenetics
JF - Cancer Genetics and Cytogenetics
IS - 2
ER -