Differential expression of MST4, STK25 and PDCD10 between benign prostatic hyperplasia and prostate cancer

前列腺增生与前列腺癌中MST4、STK25及PDCD10的差异表达

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作者:Heyu Zhang, Xi Ma, Saihui Peng, Xu Nan, Hongshan Zhao

Abstract

Both benign prostatic hyperplasia (BPH) and prostate cancer (PC) are common diseases for men around the world. Both serine/threonine protein kinase MST4 (MST4) and serine/threonine kinase 25 (STK25) belong to the Ste20-like kinases and interact with programmed cell death 10 (PDCD10) which is closely linked to cancer diseases. To clarify the roles of MST4, STK25 and PDCD10 in prostate carcinogenesis, we examined MST4, STK25 and PDCD10 expression in tissue microarray blocks containing 110 cores of BPH and 160 cores of PC immunohistochemically and evaluated their correlation with clinicopathological findings. MST4 was not expressed in all the BPH cases and expressed in 38.7% of PC cases (P < 0.0001). STK25 expression was found in 77.3% of BPH cases and 93.1% of PC cases (P < 0.0001). PDCD10 staining was considered weak in 82 (74.5%) and strong in 28 (25.5%) of BPH cases. However, in prostate cancer cases, PDCD10 staining was weak in 95 (59.4%) and strong in 65 (40.6%) (P < 0.05). PDCD10 and STK25 immunostaining were associated with age in prostatic hyperplasia cases (P < 0.05). The staining intensity for STK25 was significantly greater in Gleason grades 3-5 (47.1% of such cases staining strongly) compared with other grades of prostate cancer (only 26.5% of these cases staining strongly; P < 0.05). Our results suggest that MST4, STK25 and PDCD10 are unregulated in prostate cancer and may play roles in prostate tumorigenesis. MST4 may be a helpful marker for identifying prostate cancer.

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