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BioMed Research International
Volume 2014 (2014), Article ID 380398, 9 pages
http://dx.doi.org/10.1155/2014/380398
Research Article

KCTD11 Tumor Suppressor Gene Expression Is Reduced in Prostate Adenocarcinoma

1Department of Biotechnological and Applied Clinical Sciences, University of L’Aquila, Via Vetoio, Coppito 2, 67100 L’Aquila, Italy
2Department of Pathology, San Salvatore Hospital, 67100 L’Aquila, Italy
3Department of Molecular Medicine, “Sapienza” University of Rome, Via Regina Elena 291, 00161 Rome, Italy

Received 7 February 2014; Revised 28 April 2014; Accepted 29 April 2014; Published 19 June 2014

Academic Editor: Giovanni Luca Gravina

Copyright © 2014 Francesca Zazzeroni et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Prostate cancer is the most common noncutaneous cancer among men in the United States. A genetic contribution to prostate cancer risk has been documented, but knowledge of the molecular mechanisms involved in prostate cancer initiation is still not well understood. Loss of heterozygosity (LOH) of chromosomal regions is crucial in tumor progression. In human prostate cancer, several chromosomal regions demonstrating a high frequency of LOH have been previously identified. KCTD11 (REN) is a tumor suppressor gene mapping on human chromosome 17p13.2, whose expression is frequently lost in human medulloblastoma and in several other cancer types. KCTD11 acts as a negative regulator of the Hedgehog (Hh) signaling. Here, we demonstrated that KCTD11 LOH is a common genetic lesion in human prostate adenocarcinoma. Indeed, nuclear KCTD11 protein expression is strongly reduced in primary prostate cancer, and this event correlated with overexpression of proteins acting into the Hedgehog pathway. Low levels of KCTD11 mRNA have been also observed in prostatic cancer cells, and ectopic overexpression of KCTD11 led to growth arrest. Our study demonstrates and supports that KCTD11, as well as negatively regulated downstream effectors belonging to Hh signaling, plays a role in prostate cancer pathogenesis. This could be suitable to characterize new diagnostic and therapeutic markers.