Bladder cancer has been identified as one of the most malignant cancers with high incidence and mortality. The underlying mechanisms by which regulate the tumorigenesis of bladder cancer deserve further investigation. Here, we found that miR-192-5p was downregulated in human bladder cancer cell lines and tissues. Overexpression of miR-192-5p significantly inhibited the growth of bladder cancer cells, while depletion of miR-192-5p exerted opposite effect. Bioinformatics analysis and molecular mechanism study identified that miR-192-5p targeted the transcription factor Yin Yang 1 (YY1) and decreased the expression level of YY1. Highly expressed YY1 attenuated the potential tumor suppressive function of miR-192-5p. The expression of miR-192-5p was negatively correlated with that of YY1 in bladder cancer tissues. These results indicated that miR-192-5p might serve as a promising target in bladder cancer diagnosis and therapy.

Increasing reports have demonstrated that aberrant expression of microRNAs (miRNAs) is found in multiple human cancers. Many studies have shown that down-regulated level of miR-30a is in a variety of cancers including prostate cancer (PCa). However, the precise mechanisms of miR-30a in PCa have not been well explored. In this study, we investigated the biological functions and molecular mechanism of miR-30a in PCa cell lines, discussing whether it could be a therapeutic biomarker of PCa in the future. We found that miR-30a is down-regulated in PCa tissues and cell lines. Moreover, the low level of miR-30a was associated with increased expression of SIX1 in PCa tissues and cell lines. Up-regulation of miR-30a significantly inhibited proliferation of PCa cells. In addition, invasion of PCa cells was suppressed by overexpression of miR-30a. However, down-regulation of miR-30a promoted cell growth and invasion of PCa cells. Bioinformatics analysis predicted that the SIX1 was a potential target gene of miR-30a. Next, luciferase reporter assay confirmed that miR-30a could directly target SIX1. Consistent with the effect of miR-30a, down-regulation of SIX1 by siRNA inhibited proliferation and invasion of PCa cells. Overexpression of SIX1 in PCa cells partially reversed the effect of miR-30a mimic. In conclusion, introduction of miR-30a dramatically inhibited proliferation and invasion of PCa cells by down-regulating SIX1 expression, and that down-regulation of SIX1 was essential for inhibition of cell growth and invasion of PCa cells by overexpression of miR-30a.

Lycopene is a natural compound that alleviates oxidative stress and inflammation, exerting therapeutic effects in a number of cancers. The aim of this study is to investigate the efficacy of lycopene in inhibiting prostate cancer. Cell viability assays indicated the dose- and time-dependent toxicity of lycopene in prostate cancer cells. Annexin V/propidium iodide double-staining assays revealed the strong apoptotic effects of lycopene. The levels of inflammatory factors, including interleukin-1 (IL1), IL6, IL8, and tumor necrosis factor-α (TNF-α), in lycopene-treated cells were also reduced by lycopene treatment. With the increasing dose of lycopene, the survival of mice bearing prostate cancer xenografts was significantly improved (P < 0.01), and the tumor burden was significantly reduced (P < 0.01). Our results indicate that lycopene is a promising chemotherapy drug, which inhibits prostate cancer progression by suppressing the inflammatory response.

An increasing number of studies reported that microRNA (miR)-30a was dysregulated in several types of human cancer and may contribute to cancer carcinogenesis and progression. However, its expression and roles in renal cell carcinoma (RCC) remain unknown. In the present study, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to quantify miR-30a expression in RCC tissues and cell lines. The cell counting kit-8 assay, migration and invasion assays were used to evaluate the roles of miR-30a on the proliferation, migration and invasion of RCC cells. The target gene of miR-30a was identified by luciferase reporter assays, RT-qPCR and western blotting. The results indicated that miR-30a was downregulated in RCC tissues and cell lines compared with corresponding noncancerous tissues and normal renal cell line, respectively. Re-expression of miR-30a inhibited the proliferation, migration and invasion of RCC cells. Additionally, ADAM metallopeptidase domain 9 (ADAM9) was validated as a direct target of miR-30a. Furthermore, the knockdown of ADAM9 by small interfering RNAs was able to mimic the effects of miR-30a overexpression in RCC cells. These results highlight the important role for miR-30a in the occurrence and development of RCC, and the restoration of miR-30a might be investigated as a potential strategy for treating RCC.