Prostate cancer (PCa) has become the second leading cause of cancer‐related mortality in males worldwide. Although the long noncoding RNA DLX6‐AS1 has been recognized to be an oncogene in multiple cancers, the biological function and regulatory mechanism of DLX6‐AS1 in prostate cancer are still obscure. In the present study, we observed that DLX6‐AS1 was significantly upregulated in PCa tissues and cells. Knockdown of DLX6‐AS1 inhibited PCa progression by suppressing cell proliferation and accelerating cell apoptosis. Molecular mechanism exploration indicated that DLX6‐AS1 acted as a sponge for miR‐497‐5p and synuclein gamma (SNCG) was a downstream target gene of miR‐497‐5p. In addition, there was a negative correlation between DLX6‐AS1 and miR‐497‐5p in PCa tissues. Rescue assays showed that SNCG overexpression could partially recover DLX6‐AS1 knockdown‐mediated inhibition of progression in PCa. Furthermore, xenograft tumor model was established to determine the role of DLX6‐AS1 in PCa tumor growth and the results suggested that DLX6‐AS1 could facilitate tumor growth by regulating SNCG in vivo. In conclusion, our study investigated the biological function and underlying mechanism of DLX6‐AS1 in PCa and validated that DLX6‐AS1 functioned as an oncogene through miR‐497‐5p/SNCG axis.

Research has shown that the incidence of prostate cancer is increased in patients with type 2 diabetes mellitus (T2DM) 1. Glucagon-like peptide-1 (GLP-1) is a gastrointestinal hormone that enhances glucose-dependent insulin secretion and suppresses glucagon release. Here, we examined the effect of exenatide and liraglutide, 2 types of GLP-1 analogues, on prostate cancer cells growth by CCK-8 assay, Hoechst33258 staining assay, and western blot analysis of apoptosis-related proteins Bax and Bcl-2. Also the kinase pathways maybe involved and the expression of GLP-1 receptor (GLP-1 R) in LNCap cells was detected. In our experiments, exenatide and liraglutide significantly inhibited the proliferation of the LNCap cell lines and induced the cell apoptosis. Exenatide (1-100 nmol/L) increased the ratio of Bax/Bcl-2 in a dose-dependent manner, whereas liraglutide increased Bax/Bcl-2 ratio only at concentrations of 10 nmol/L. And we found that GLP-1 analogues activate p38 but not ERK1/2 or AKT in LNCap cells. And classical GLP-1 receptor was detected in LNCap cells. These data suggest that exenatide and liraglutide attenuate prostate cancer growth through regulating P38 pathway by binding with GLP-1R.

Prostate cancer (PCa) is known as one of the most common cancers in men all over the world. Previous studies have identified that the pro-inflammatory mediator interleukin-17F (IL-17F) aggravates the progression of several diseases. However, whether IL-17F plays a role in PCa is still lack of enough exploration. In this study, IL-17F expression was strikingly upregulated in PCa tissues. Treatment of IL-17F promoted cell viability at a dose-dependent manner. Further, functional assays were implemented by treatment of 100 ng/ml of IL-17F. Cell viability, proliferation, migration, invasion and stemness were promoted by 100 ng/ml of IL-17F. IL-17F increased the expression of p-PI3K and p-AKT in PCa cells, indicating that IL-17F might activate the PI3K/AKT signalling pathway in PCa cells. LY294002 (the inhibitor of the PI3K/AKT signalling pathway) could reverse the facilitating effects of IL-17F treatment on PCa cell viability, proliferation, migration, invasion and stemness. Taken together, current study revealed that IL-17F facilitated PCa cell malignant phenotypes via activation of the PI3K/AKT signalling pathway, offering a potential therapeutic target for PCa.