This study investigates whether the anti-metastasis effect of microRNA-139 (miR-139) on hepatocellular carcinoma (HCC) is mediated through regulating c-fos expression. The expression levels of miR-139 and c-fos in human HCC cell sublines with high (MHCC97H) and low (MHCC97L) spontaneous metastatic potentials were quantified using QPCR or Western blot. miR-139 mimics was transfected into MHCC97H cells to overexpress miR-139, and miR-139 inhibitor was transfected into MHCC97L cells to down-express miR-139. The effect of overexpression or down-expression of miR-139 on c-fos expression of MHCC97H and MHCC97L cells was evaluated using QPCR and Western blot. The 3' untranslated region segments of FOS containing the miR-139 binding sites were amplified by PCR, and the luciferase activity in the transfected cells was assayed. In comparison with the expression level of miR-139 in MHCC97L cells, the expression level in MHCC97H cells was significantly decreased, whereas c-Fos was significantly up-regulated in MHCC97H. The overexpression of miR-139 significantly inhibited the expression of c-fos in MHCC97H cells, and the down-expression of miR-139 significantly promoted the expression of c-fos in MHCC97L cells. miR-139 suppressed the luciferase activity of the pGL-FOS by approximately 40% compared with the negative control. In vitro cell migration analysis demonstrated that depletion of c-fos or overexpression of miR-139 in MHCC97H cells reduced cell migration, whereas overexpression of c-fos or depletion of miR-139 in MHCC97L cells increased cell migration. Thus, we got the conclusion that miR-139 expression is down-regulated in human HCC cell sublines with high spontaneous metastatic potentials (MHCC97H). Derepression of c-Fos caused by miR-139 down-regulation contributes to the metastasis of HCC.

Objective: Clinical studies evaluating effectiveness and safety of cryosurgery (CS) for clinically localized prostate cancer (PCa) have reported conflicting results. We aim to obtain systematic and comprehensive evidence regarding the potential benefits and safety of CS compared with those of radiotherapy (RT) and radical prostatectomy (RP), respectively. Methods: All controlled trials comparing CS with RT or RP and single-arm studies reporting results of CS therapy were identified through comprehensive searches of PubMed, the Cochrane Library and Embase, and a metaanalysis and systematic review of these studies were chosen. Results: Ten publications from seven trials, with a total of 1,252 patients, were included for meta-analysis, which revealed no significant differences in comparisons of CS vs. RT and CS vs. RP for overall survival (OS), diseasespecific survival (DSS) and biochemical disease-free survival (bDFS), except for a significantly lower bDFS for CS than RP [risk ratio (RR) 0.85, 95% confidence interval (CI) 0.73-0.99, P=0.03]. Moreover, dynamic analysis of pooled complications in months of 1, 3, 6, 12 and 24 demonstrated significantly a higher occurrence for urinary and sexual bothers in CS then RT at most disease stages. Furthermore, a systematic review of the literature focusing on comparative data of databases and materials of single-arm trials revealed satisfactory survival results in both primary and salvage CS. Furthermore, following CS, we observed an increasing incidence of 41% compared to which in the initial phase and maximum overall value of >53.3% for urinary complications; similarly, we observed an increasing incidence of 56.8% and a maximum overall value of 100% for erectile dysfunction. Conclusions: Our results showed that CS could be an effective method for clinically localised PCa with survival results satisfactory and comparable to other modalities. However, the large percentage of complications caused by CS should be carefully monitored. Additional high-quality, well-designed randomised controlled trials and comparative studies with long-term follow-up results are required to define the options for patients with clinically localised PCa.

miR-200b-3p is down-regulated by low expression of p73 in AIPC cells, and this interaction contributes to the proliferation of AIPC.