Background Human bladder cancer is one of the common malignant tumors, and it mainly occurs in men. miR-182-5p, a member of miR-183 family, acts as tumor suppressor or oncogene in various kinds of tumors. In this study, we first investigate that the absence of miR-182-5p in human bladder cancer promotes tumor growth by regulating the expression of Cofilin 1, an actin modulating-protein. Methods Human bladder tumor tissue specimens were collected to detect the expression of miR-182-5p and Cofilin 1 by qRT-PCR. Luciferase activity assay was performed to demonstrate the regulation of Cofilin 1 mRNA 3′UTR by miR-182-5p. Then, cell experiments were performed to analysis the effect of miR-182-5p/Cofilin 1 pathway on tumor cell proliferation, migration, invasion and colony forming efficiency. Finally, xenograft tumor models were established to evaluate the role of miR-182-5p in tumorigenesis abilities in vivo. Results qRT-PCR and Western blotting analysis showed that Cofilin 1 expression was up-regulated in both bladder cancer tissues and cell lines compared with normal. Luciferase activity assay showed that miR-182-5p specifically targets Cofilin 1 mRNA 3′UTR and represses the expression of Cofilin 1. Also, miR-182-5p inhibited bladder tumor cell proliferation, migration, invasion and colony forming efficiency. Furthermore, xenograft tumor model assay showed that miR-182-5p plays a negative role in bladder cancer tumorigenesis abilities in vivo. Conclusion Present results suggest that miR-182-5p could inhibit human bladder tumor growth by repressing Cofilin 1 expression. Our findings may provide a new horizon for exploring therapeutic target of bladder cancer.

Purpose Genetic factors play an indispensable role in the pathogenesis of lifelong premature ejaculation (LPE). The susceptibility genes/SNPs that have been discovered are very limited and can only explain part of the genetic effects of LPE. Therefore, discovering more genetic polymorphisms associated with the occurrence and development of LPE will help reveal the pathogenesis of LPE. Materials and Methods We conducted a genome-wide association study of LPE in 486 Chinese male Han people (cases and controls). We used Gene Titan multi-channel instrument and Axiom Analysis Suite 6.0 software for genotyping. Imputation was performed by IMPUTE2 software and the 1000 Genomes Project (Phase3) was used as reference for haplotype. Finally, logistic regression analysis was performed on all loci that passed the quality control. The odds ratio and 95% confidence interval were calculated to determine the association between each SNPs and Chinese male Han population LPE risk. Results The results showed that a total of 33 genetic variants in 13 genes ( LACTBL1 , SSBP3 , ACOT11 , LINC02486 , TMEM154 , LINC01098 , NONE , HCG27 , HLA-C , TNFSF8 , TNC , FAM53B , SULF2 ) have a suggestively significant genome-wide association with LPE risk (p<5×10 −6 ). Conclusions This study is the first to conduct a GWAS on LPE in Chinese male Han population 33 genetic polymorphisms have a suggestive genome-wide association with LPE risk. This study have provided data supplement for the genetic loci of LPE risk, and laid a scientific foundation for the pathogenesis and the targeted therapy of LPE.

Premature ejaculation (PE) is considered to be one of the most common sexual dysfunction disorders in males with an incidence of 3%-30% (Goldstein, 2003; Huang et al., 2016). PE has a serious impact on patient's work and life, such as physical and mental health, and the relationships with their partner and/ or spouse (Serefoglu et al., 2014). Generally, PE can be divided into acquired PE (APE) and lifelong PE (LPE), among which LPE is one of the most widespread types of PE in males, accounting for about 20%-30% of the male population (Gillman & Gillman, 2019; Laumann et al., 2005). The latest definition of LPE is that ejaculation always or almost always occurs before or within the l min of vaginal penetration at the beginning of the first sex, and there is no control over ejaculation for each or almost every time and negative emotions such as depression, irritability, depression and/or avoidance of sexual contact (Serefoglu et al., 2014). Although some psychological, behavioural and biological aetiologies have been proposed, the exact pathophysiology of LPE remains unclear.