Prostate cancer (PCa) is one of the major men’s malignancies with high mortality worldwide. Circular RNAs (circRNAs) have been shown to serve as essential regulators in human cancers. CircRNA can exert their functions by cooperating with their host genes. In the present study, microarray analysis revealed an upregulated mRNA in PCa samples. X-linked inhibitor of apoptosis protein (XIAP), a key regulator in the progression of human cancers. Through bioinformatics analysis, we determined that XIAP is a host gene for circRNA0005276. Therefore, this study focused on the interaction between circ0005276 and XIAP as well as their functions in PCa progression. The upregulation of XIAP and circ0005276 was determined in PCa tissues and cell lines. Moreover, we confirmed the positive regulation of circ0005276 on XIAP expression. Functionally, we validated that circ0005276 and XIAP promoted cell proliferation, migration and epithelial–mesenchymal transition. Mechanistically, we verified that circ0005276 interacted with FUS binding protein (FUS) so as to activate the transcription of XIAP. Rescue assays were conducted to determine the crucial role of XIAP in circ0005276 and FUS-mediated PCa cellular processes. Collectively, our study revealed the mechanism and function of circ0005276 and its host gene XIAP in PCa progression.

Curcumin is known to exhibit anticancer effects on various cancers with selective cytotoxicity in tumor cells. In the present study, the effects of curcumin-induced multiple PCDs on human non-small cell lung cancer (NSCLC) cells and the potential molecular mechanisms of apoptosis and autophagy triggered by curcumin via the PI3K/Akt/mTOR signaling pathway were explored, further confirmed by co-culture of curcumin with mTOR blocker rapamycin and PI3K/Akt inhibitor LY294002. The anti-proliferation effect of different stimulus was measured by MTT assay. Apoptosis was detected by flow cytometry. Autophagy induction was detected by MDC labeling and western blotting of Beclin1, LC3, and p62 expression. The mRNA and protein expression levels of Akt and mTOR were assayed by real-time fluorescence quantitative (qRT-PCR) technique and western blotting. Our results showed that curcumin inhibited the viability of A549 cells time-and dose-dependently. In addition, a dosage-dependent A549 cell apoptosis-induction phenomena was observed by the curcumin intervention. Moreover, obvious autophagy was induced after curcumin-treatment, characterized by the formation of fluorescent particles [autophagic vesicles (AVs)] and significant increase in ratio of LC3-Ⅱ/LC3-Ⅰ and Beclin1 as well as decreased p62 expression. Furthermore, the effect of curcumin on a substantial downregulation of phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway was observed. It is worth noting that the inhibition of mTOR by rapamycin or of PI3K/Akt by LY294002 augmented curcumin-induced apoptosis and autophagy, leading to significant inhibition of cell proliferation. From these findings, it can be speculated that curcumin potently inhibit the cell growth of NSCLC A549 cells through inducing both apoptosis and autophagy by inhibition of the PI3K/Akt/mTOR pathway. These results support the potential use of curcumin as a novel candidate in treatment of human lung cancer.

Resveratrol (RSV) has been reported to induce autophagy and apoptosis in non-small-cell lung cancer A549 cells, and the nerve growth factor receptor (NGFR) regulates autophagy and apoptosis in many other cells. However, the effect of NGFR on autophagy and apoptosis induced by RSV in A549 cells remains unclear. Here, we found that RSV reduced the cell survival rate in time- and concentration-dependent manners, activating autophagy and apoptosis. Lethal autophagy was triggered by RSV higher than 55 μM. The relationship between autophagy and apoptosis depended on the type of autophagy. Specifically, mutual promotion was observed between apoptosis and lethal autophagy. Conversely, cytoprotective autophagy facilitated apoptosis but was unaffected by apoptosis. RSV enhanced NGFR by increasing mRNA expression and prolonging the lifespan of NGFR mRNA and proteins. RSV antagonized the enhanced autophagy and apoptosis caused by NGFR knockdown. As the downstream pathway of NGFR, AMPK-mTOR played a positive role in RSV-induced autophagy and apoptosis. Overall, RSV-induced autophagy and apoptosis in A549 cells are regulated by the NGFR-AMPK-mTOR signaling pathway.

Although air pollution is a known fundamental problem in China, few studies have investigated the associations between ambient air pollution and respiratory mortality in non-metropolitan cities of China. The study aimed to investigate a potential relationship between short-term exposure to ambient air pollutants and respiratory mortality in Xi’an, China. Daily averages of PM2.5, SO2, O3, temperature, relative humidity and daily counts of respiratory mortality were obtained (2014–2016). Using a single and multi-pollutant approach in time-series analysis, the generalized additive model with natural splines was used for analysis. Subgroup analysis stratified by gender and age group (≤ 64 years and ≥ 65 years) was conducted. Seven thousand nine hundred sixty-five cases of respiratory mortality were assessed, with 62.9, 28.5, and 8.6% of mortality attributed to chronic lower respiratory diseases, influenza and pneumonia, as well as other forms of respiratory diseases, respectively. Observed pollutants were significantly associated with respiratory mortality. In the single pollutant model, 10 μg/m3 increase in a two-day moving average of PM2.5, and SO2 concentrations were significantly associated with relative risk 1.313(1.032, 1.708) and 1.4020(0.827, 2.854) of respiratory mortality, respectively. The effects of both air pollutants remained statistically significant after adjusting for collinearity in the multi-pollutant model. Ozone was only statistically associated with respiratory mortality in females at lag 0 [RR: 0.964(0.938, 0.991)]. This study provided evidence that respiratory mortality in Xi’an was significantly associated with exposure to ambient air pollutants from 2014 to 2016.