Previous literature exists on the role of microRNA (miR)-132 in initiation and progression of various malignancies. In this study, we aimed at understanding the relationship of miR-132 of prostate tumorigenesis. We collected 32 prostate cancer tissues and adjacent non-cancerous controls, and detected the expression level of miR-132. Then the miRNA database was searched online and luciferase assay perform to understand the regulatory relationship between miR-132 and E2F5. Moreover, we also conducted real-time PCR and western blot analysis to study the mRNA and protein expression level of E2F5 among different groups (cancerous tissue, n=32; non-cancerous tissue, n=32) or cells treated with scramble control, miR-132 mimics, E2F5 siRNA and miR-132 inhibitors. miR-132 was upregulated in cancerous tissues of prostate cancer patients. E2F5 was the target of miR-132, and negative regulatory relationship between miR-132 and E2F5 was also confirmed by luciferase assay. The mRNA and protein expression level of E2F5 increased in cancerous tissue group. miR-132 decreased the expression of E2F5 in prostate cancer cells, and introduction of miR-132 reduced the viability and E2F5 and promoted the viability of prostate cancer cells. miR-132 inhibited apoptosis and E2F5 accelerated apoptosis. In conclusion, miR-132 was upregulated in cancerous tissue of prostate cancer. E2F5 was a direct target of miR-132, and downregulation of E2F5 caused by upregulation of miR-132 may contribute to the tumorigenesis of prostate cancer.

Background Cell division cycle associated 4 (CDCA4) has been reported to be engaged into the progression of several cancers. The function of CDCA4 in Non-small cell lung cancer (NSCLC) was unknown. We aimed to explore the critical role of CDCA4 in NSCLC. Methods CDCA4 stably knocking down and overexpression cell lines were established and Western blotting assay was applied to measure relevant protein expression of Epithelial-Mesenchymal Transtion (EMT) and cell autophagy. Staining of acidic vacuoles, transmission electron microscopy and immunofluorescence staining were employed to detect autophagy. The ability of cells to migrate and invade were detected by Transwell migration and invasion assays. The interaction of CDCA4 with CARM1 was identified by immunoprecipitation and Western blotting analysis. Results In the present study, it was found that inhibition of CDCA4 induced EMT, migration and invasion of NSCLC cells while inhibiting autophagy of NSCLC cells. Meanwhile, overexpression of CDCA4 in NSCLC cells showed the opposite function. More importantly, the inhibition of autophagy could promote the EMT, migration and invasion of NSCLC cells, which should be impaired via the activation of autophagy. In addition, CDCA4-inhibited EMT, migration and invasion could be partially aggravated by autophagy activator, rapamycin, and reversed by autophagy inhibitor, 3-MA. Correspondingly, the application of rapamycin or 3-MA to CDCA4 knockdown cells showed the opposite effects. Further investigation suggested that CDCA4 could interact with coactivator associated arginine methyltransferase 1 (CARM1). Autophagy was induced while cell migration and invasion were inhibited in CARM1 knockdown cells. CDCA4 could suppress the protein expression CARM1 and knocking down of CARM1 could alter cell autophagy, migratory and invasive abilities regulated by CDCA4. Conclusion All data indicated that CDCA4 inhibited the EMT, migration and invasion of NSCLC via interacting with CARM1 to modulate autophagy.

This research aimed to analyze lifestyle-related factors which influence Helicobacter pylori (Hp) infection and outcomes in Chinese adults. A single-center, retrospective study was performed from January 2012 to December 2020. Self-administered questionnaires were used to collect relevant lifestyle information, and the 13C-urea breath test was used to diagnose active Hp infection. A total of 18,211 subjects were enrolled in the study, of which 5,511 were females (30.26%). Subjects were studied longitudinally for up to five follow-up visits. At baseline, gastric Hp test was negative in 10,670 subjects (58.59%) and positive in 7,541 subjects (41.41%). Males exhibited a significantly higher Hp infection rate than females (38.56% vs 2.65%, respectively; χ 2 = 26.45, P < 0.001). Throughout the course of follow-up, Hp positive rates in the subjects decreased ( χ trend 2 {\chi }_{\text{trend}}^{2} = 666.04, P < 0.001). Among the subjects with baseline negative results, 3–6% changed from negative to positive during follow-up. In contrast, among those with baseline positive results, >70% remained positive, and 21–26% changed from positive to negative. However, only 22–27% of Hp-infected subjects received pharmacotherapy. The results indicate the prevalence of Hp infection is high in the Chinese population. That additional effort is required to prevent and control Hp infection.

Background: The association between lifestyle factors and the risk of colon adenomas and serrated polyps (SPs) in the in asymptomatic healthy people is unclear. Aims: The aim of this study was to explore and compare the lifestyle-related risk factors related to colon adenomas and SPs on average-risk individuals. Methods: A total of 5736 subjects，namely, 4346 men (75.77%) and 1390 women (24.23%), with an average age of 48.60 ± 7.29 years were included. Subjects underwent colonoscopy and provided diet and lifestyle data for 5 years. Results: We documented the data of 555 conventional adenomas, 324 SPs, and 95 synchronous adenomas and SPs. Logistic regression analysis indicated smoking, middle age, overweight and high education level was common risk factors for adenomas and SPs. Smokers were more likely to develop adenomas (OR: 1.41, 95%CI: 1.29-1.54) and SPs (OR: 1.62, 95%CI: 1.46-1.81), respectively. The risk of adenomas and SPs in middle-aged adults was 1.92 (OR: 1.92, 95%CI: 1.55-2.37) and 1.36 fold (OR: 1.36, [95%CI: 1.07-1.73]) compared with young adults, respectively. SPs were more strongly correlated with BMI than adenomas (P<0.05). Those with a high educational background had a higher risk of conventional adenomas (OR: 1.13, 95% CI: 0.99-1.29) and SPs (OR: 1.13, 95% CI: 0.96-1.31) compared to individuals with a low educational background. Men and fasting blood glucose ≥ 7.0 mmol/L were associated with higher risk of adenomas. Conclusions: Lifestyle risk factors have different association with adenomas or SPs. These findings provide new clues for the prevention of colorectal polyps.