A number of previous studies have reported that dysregulated miR-184 expression is associated with the development of cancer. The aim of the present study was to investigate the role of miR-184 in prostate cancer (PC) and the mechanism underlying its effects. Data from human tumor tissue samples were collected from The CEancer Genome Atlas to determine the expression levels of miR-184 and DLX1. The miR-184 mimic and pcDNA3.1-DLX1 plasmid were utilized to induce overexpression of miR-184 and DLX1 in Du145 cells, respectively. Cell Counting Kit-8, wound healing and Transwell assays were performed to examine the effects of miR-184 on the aggressiveness of PC cells. Dual-luciferase reporter gene assay was used to investigate the association between miR-184 and DLX1, and reverse transcription-quantitative PCR and western blot analyses were utilized to determine the mRNA and protein levels. miR-184 expression was found to be downregulated whereas DLX1 was upregulated in PC tissues compared with normal prostate tissues. Cell propagation, migration and invasion were all inhibited by miR-184 upregulation in Du145 cells. Dual luciferase reporter assay confirmed the association between miR-184 and DLX1. The inhibitory effect of miR-184 mimic on cell behaviors was reversed by upregulation of DLX1. These findings suggest that miR-184 plays a beneficial role in suppressing the tumorigenesis of PC by directly targeting DLX1, and it may represent a potential therapeutic strategy for PC.

Background Genes are differentially expressed in diabetes induced erectile dysfunction (DED); however, there is still a lack of systematic and in-depth understanding of the cellular and molecular mechanisms of DED. This study aimed to systematically analyze molecular correlates leading to ED in diabetes by bioinformatics analysis, and provide new insights into the mechanism of DED. Results A total of 800 differentially expressed genes (DEGs, 407 upregulated and 393 downregulated) were identified in the diabetic-induced ED samples compared with the control group. The upregulated DEGs were mainly enriched in glucose and lipid metabolism-related pathways, and the downregulated DEGs were primarily enriched in tissue development and structure. The dysregulated extracellular matrix genes (especially related to collagen and elastin) may be closely related to the damage of erectile function of the corpus cavernosum. Sixteen hub genes (6 upregulated, 10 downregulated) and 24 modules were detected buy hub gene and MCODE analysis. Protein phosphorylation might play an important role in DED. Furthermore, 20 TFs targeting DEGs were identified by ChEA3. Conclusions Our research comprehensively and systematically described the molecular characteristics of DED, and suggested that dysregulated extracellular matrix genes and protein phosphorylation may play critical roles in DED.

Background: Genes are differentially expressed in diabetes induced erectile dysfunction (DED); however, there is still a lack of systematic and in-depth understanding of the cellular and molecular mechanisms of DED. This study aimed to systematically analyze molecular correlates leading to ED in diabetes by bioinformatics analysis, and provide new insights into the mechanism of DED.Results: A total of 800 differentially expressed genes (DEGs, 407 upregulated and 393 downregulated) were identified in the diabetic-induced ED samples compared with the control group. The upregulated DEGs were mainly enriched in glucose and lipid metabolism-related pathways, and the downregulated DEGs were primarily enriched in tissue development and structure. The dysregulated extracellular matrix genes (especially related to collagen and elastin) may be closely related to the damage of erectile function of the corpus cavernosum. Sixteen hub genes (6 upregulated, 10 downregulated) and 24 modules were detected buy hub gene and MCODE analysis. Protein phosphorylation might play an important role in DED. Furthermore, 20 TFs targeting DEGs were identified by ChEA3.Conclusions: Our research comprehensively and systematically described the molecular characteristics of DED, and suggested that dysregulated extracellular matrix genes and protein phosphorylation may play critical roles in DED.

Diabetes can cause erectile dysfunction (ED) in more than half of male patients. However, the mechanisms underlying diabetes-induced erectile dysfunction (DED) remain unknown. This study is aimed at systematically analyzing the cellular and molecular mechanisms leading to DED using bioinformatic analysis and providing molecular targets for predicting and treating DED. In total, we identified 800 DEGs in the DED samples compared with those in the control group. The 407 upregulated DEGs were mainly enriched in glucose and lipid metabolism-related pathways, and the 393 downregulated DEGs were primarily enriched in tissue development and structure. Dysregulated extracellular matrix genes (especially collagen and elastin) may be closely related to damage to the erectile function of the corpus cavernosum. Sixteen hub genes and 24 modules were detected with hub genes and MCODE analysis. The consensus sequence AAA (G/C) AAA was observed at the promoter sites of most genes that were enriched in the “posttranslational protein phosphorylation” pathway. These genes had abundant phosphorylation sites. Furthermore, 20 TFs targeting DEGs were identified using ChEA3 tool. In conclusion, our research comprehensively and systematically describes the molecular characteristics of DED and suggests that dysregulated extracellular matrix genes and protein phosphorylation may play critical roles in DED. Therefore, they may be potential markers for diagnosing and treating DED.