Resveratrol (RSV) is a natural polyphenol that is known as a powerful chemopreventive and chemotherapeutic anticancer molecule. This study focused on the effects of RSV on the activities and expression levels of antioxidant enzymes in the cancer cells. Prostate cancer PC-3 cells, hepatic cancer HepG2 cells, breast cancer MCF-7 cells and the non-cancerous HEK293T kidney epithelial cells were treated with a wide range of RSV concentrations (10-100 μM) for 24-72 h. Cell growth was estimated by trypan blue staining, activities of the antioxidant enzymes were measured spectrophotometrically, expression levels of the antioxidant enzymes were quantified by digitalizing the protein band intensities on Western blots, and the percentage of apoptotic cells was determined by flow cytometry. Treatment with a low concentration of RSV (25 μM) significantly increased superoxide dismutase (SOD) activity in PC-3, HepG2 and MCF-7 cells, but not in HEK293T cells. Catalase (CAT) activity was increased in HepG2 cells, but no effect was found on glutathione peroxidase (GPX) upon RSV treatment. RSV-induced SOD2 expression was observed in cancer cells, although the expression of SOD1, CAT and GPX1 was unaffected. Apoptosis increased upon RSV treatment of cancer cells, especially in PC-3 and HepG2 cells. Together, our data demonstrated that RSV inhibits cancer cell growth with minimal effects on non-cancerous cells. We postulate that the disproportional up-regulation of SOD, CAT and GPX expression and enzymatic activity in cancer cells results in the mitochondrial accumulation of H2O2, which in turn induces cancer cell apoptosis.

Prostate cancer is one of the life threatening disorders of male. Although, over the last two decades, a high rate of overdiagnosis, and overtreatment has lowered the incidence rate of prostate cancer, the treatment or prevention strategies are not enough to control the high rate of disease related mortality. Current medical treatment approaches include surgery, radiation therapy, chemotherapy, hormonal therapy, cryosurgery and other methods. These approaches are more or less effective either as monotherapy or in multimodal approach. However, many adverse or side effects exist with these strategies. Researches are ongoing to find out the way or better strategies to eliminate the adverse effects. Dietary modifications may also contribute to decrease prostate cancer risk. Several nutraceuticals against prostate cancer have also been identified. This review article summarizes some of the current treatment, and prevention strategies with the protection of prostate cancer, which may be helpful to control and prevent this highly frequent life threatening disease.

BackgroundThe abnormal expression of non-coding RNAs (ncRNAs), such as microRNAs and long ncRNAs, often contribute to the development of cancers. miR-200c functions as a tumour suppressor that impacts the growth of bladder cancer cells and the epithelial-to-mesenchymal transition (EMT). LncRNA X inactive specific transcript (XIST) is highly expressed in tumour tissues, promotes cancer progression and might act as an miRNA molecular sponge. This study aimed to examine the relationship between lncRNA XIST and miR-200c and to assess their functions in the regulation of the stemness properties and tumourigenicity of human bladder cancer stem cell (BCSC)-like cells.MethodsBiological effects including cell clone formation, sphere formation, self-renewal properties and mouse tumourigenesis were examined in BCSC-like cells with miR-200c overexpression or XIST knockdown. Real-time PCR and western blotting were used to detect the expression changing of related factors in BCSC-like cells gene models. Dual luciferase reporter assay was used to examine the changes of XIST and miR-200c expression levels.ResultsThe results indicated that miR-200c overexpression and XIST knockdown could inhibit cell clone formation, self-renewal ability and EMT in BCSC-like cells. miR-200c knockdown could restore the tumour growth inhibition caused by XIST knockdown.ConclusionLncRNA XIST may act as an inhibitor of miR-200c to regulate the stemness properties and tumourigenicity of bladder cancer cells, and our findings might reveal a potential strategy of targeting XIST for bladder cancer therapy.Electronic supplementary materialThe online version of this article (10.1186/s12935-018-0540-0) contains supplementary material, which is available to authorized users.

Ubiquitination is a post-translational modification process that regulates multiple cell functions. It also plays important roles in the development of cancer. Mechanistically, ubiquitination is a complex process that is comprised of a series of events involving ubiquitin-activating enzymes, ubiquitin-conjugating enzymes and ubiquitin ligases. In general, covalent attachment of ubiquitin to the target proteins marks them for degradation. Dysregulation of the ubiquitination process may cause carcinogenesis. In this review, we summarize recent developments in understanding the relationship between ubiquitination enzymes and carcinogenesis.