Prostate cancer is the most common noncutaneous cancer among men in the United States. A genetic contribution to prostate\ncancer risk has been documented, but knowledge of the molecular mechanisms involved in prostate cancer initiation is still not\nwell understood. Loss of heterozygosity (LOH) of chromosomal regions is crucial in tumor progression. In human prostate cancer,\nseveral chromosomal regions demonstrating a high frequency of LOH have been previously identified. KCTD11 (REN) is a tumor\nsuppressor gene mapping on human chromosome 17p13.2, whose expression is frequently lost in human medulloblastoma and\nin several other cancer types. KCTD11 acts as a negative regulator of the Hedgehog (Hh) signaling. Here, we demonstrated that\nKCTD11 LOH is a common genetic lesion in human prostate adenocarcinoma. Indeed, nuclear KCTD11 protein expression is\nstrongly reduced in primary prostate cancer, and this event correlated with overexpression of proteins acting into the Hedgehog\npathway. Low levels of KCTD11 mRNA have been also observed in prostatic cancer cells, and ectopic overexpression of KCTD11 led\nto growth arrest.Our study demonstrates and supports that KCTD11, as well as negatively regulated downstreameffectors belonging\nto Hh signaling, plays a role in prostate cancer pathogenesis. This could be suitable to characterize new diagnostic and therapeutic\nmarkers.
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