Shengsong Huang

MiR-203 down-regulates Rap1A and suppresses cell proliferation, adhesion and invasion in prostate cancer

ObjectiveEvidence supports an important role for miR-203 in the regulation of the proliferation, migration and invasion of prostate cancer (PCa) cells. However, the exact mechanisms of miR-203 in PCa are not entirely clear.MethodsWe examined the expression of miR-203 in prostate cancer tissues, adjacent normal tissues, PCa cell lines and normal prostate epithelial cells by qRT-PCR. Then, the effects of miR-203 or Rap1A on proliferation, adhesion and invasion of PCa cells were assayed using CKK-8, adhesion analysis, and transwell invasion assays. Luciferase reporter assay was performed to assess miR-203 binding to Rap1A mRNA. Tumor growth was assessed by subcutaneous inoculation of cells into BALB/c nude mice.ResultsHere, we confirmed that the expression of miR-203 was significantly downregulated in prostate cancer specimens compared with matched adjacent normal prostate specimens. Mechanistic dissection revealed that miR-203 mediated cell proliferation, adhesion and invasion in vitro, and tumor growth in vivo, as evidenced by reduced RAC1, p-PAK1, and p-MEK1 expression. In addition, we identified Rap1A as a direct target suppressed by miR-203, and there was an inverse relationship between the expression of miR-203 and Rap1A in PCa. Knockdown of Rap1A phenocopied the effects of miR-203 on PCa cell growth and invasion. Furthermore, Rap1A over-expression in PCa cells partially reversed the effects of miR-203-expression on cell adhesion and invasion.ConclusionsThese findings provide further evidence that a crucial role for miR-203 in inhibiting metastasis of PCa through the suppression of Rap1A expression.

Prognostic impact of SUMO-specific protease 1 (SENP1) in prostate cancer patients undergoing radical prostatectomy

OBJECTIVES To investigate small ubiquitin-like modifier (SUMO)-specific protease 1 (SENP1) expression in human prostate cancer (CaP) cells and its prognostic value for CaP patients after radical prostatectomy (RP). MATERIALS AND METHODS SENP1 expression in CaP cells was detected by quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and Western blotting. By using immunohistochemistry coupled with the tissue microarray (TMA) technique, we examined SENP1 protein expression in 115 specimens of CaP, 19 prostatic intra-epithelial neoplasia (PIN) tissues, and 24 normal prostate tissues. Moreover, correlations between SENP1 protein expression, clinicopathologic features, and prognosis were statistically analyzed. RESULTS Three CaP cells, DU145, PC-3, and LNCaP had overexpression of SENP1 mRNA and protein, while the nontransformed immortalized prostate cell RWPE-1 had relatively weak SENP1 expression. Especially, DU145, a hormone-independent CaP cell line, showed higher transcriptional and translational level of SENP1 than the others. SENP1 protein expression correlated with some clinicopathologic parameters, such as pathologic stage, Gleason score, and biochemical recurrence (BCR). Positive SENP1 immunostaining in the CaP, PIN, and normal prostate tissue samples were 76.5%, 57.9%, and 4.2%, respectively. CaP patients undergoing RP with positive SENP1 expression were significantly associated with poor biochemical-free survival. Multivariate analysis indicated that SENP1 protein expression was an independent prognostic factor for BCR-free survival after RP. CONCLUSIONS This study confirmed the up-regulation of SENP1 mRNA and protein level in CaP cells. We suggested that SENP1 expression might contribute to the malignant progression of CaP. Importantly, SENP1 presented as a potential prognostic factor for BCR after RP.

Overexpression of high mobility group box 1 with poor prognosis in patients after radical prostatectomy

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