JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
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Promoter hypermethylation of SOX11 correlates with adverse clinicopathological features of human prostate cancer.

Currently available tools for early diagnosis and prognosis of prostate cancer lack sufficient accuracy. There is a need to identify novel biomarkers for this common malignancy. SOX family genes play an important role in embryogenesis and are also implicated in various cancers. SOX11 has been recently recognized as a potential tumour suppressor that is downregulated in prostate cancer. We hypothesized that hypermethylation may be responsible for SOX11 silencing in human prostate cancer. The aim of the study was to investigate SOX11 promoter methylation in prostate adenocarcinoma by comparing it with benign prostatic hyperplasia (BPH). A total of 143 human prostate tissue samples, 62 from patients with prostate cancer and 81 from patients with BPH were examined by methylation-specific PCR. Associations between SOX11 promoter methylation and clinicopathological parameters were assessed by univariate statistics. Detection rates of SOX11 promoter methylation were 80.6% and 35.8% in prostate cancer and BPH respectively (P < 0.001). SOX11 hypermethylation was associated with adverse clinicopathological characteristics of prostate cancer, including higher PSA level (P < 0.01), Gleason score ≥ 7 (P = 0.03) and perineural invasion (P = 0.03). SOX11 methylation was positively correlated with the PSA level (P = 0.001). Our data indicated that SOX11 can be a promising methylation marker candidate for differential diagnosis and risk stratification for prostate cancer.

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