Overexpressing miR-335 inhibits DU145 cell proliferation by targeting early growth response 3 in prostate cancer

MicroRNA-335 (miR-335) was reported to suppress cell proliferation in prostate cancer (PC), a common malignancy in males. The expression of early growth response 3 (EGR3) was determined to be elevated in human PC tissues; however, the possible effects and underlying mechanism of miR-335 on PC remains unknown. In the present study, miR-335 mimics and miR-335 inhibitors were respectively transfected into DU145 cells. Stable silencing of EGR3 was observed in DU145 cells following transfection with small interfering RNA. We also used Cell Counting Kit-8 and in vitro angiogenesis assays to determine the viability and revascularization potential of DU145 cells. The expression levels of EGR and caspase-3 activity were analyzed by immunohistochemistry and immunocytochemistry, respectively. We predicted the target of miR-335 by bioinformatics analysis and a dual-luciferase reporter gene assay. Western blot and quantitative real-time polymerase chain reaction analyses were performed to determine the protein and mRNA expression of molecules. miR-335 expression was downregulated in PC tissues and cell lines. Overexpression of miR-335 significantly reduced the viability and the formation of regenerative tubes of DU145 cells, and inhibited the expression of inflammatory factors. EGR3 was proposed as a possible target of miR-335, and was negatively regulated by miR-335. Silencing EGR3 suppressed the viability and angiogenesis of DU145 cells, and reduced the activity of caspase-3 and inflammatory factor expression. miR-335 inhibition along with EGR3 silencing EGR3 inhibited the cell proliferation. Furthermore, miR-335 inhibited the formation of a PC solid tumor xenograft in vivo. Thus, miR-335 may exert an antitumor effect on DU145 cells by regulating the expression of EGR3. The findings of the present study may provide insight into a novel therapeutic strategy for the treatment of prostatic carcinoma.