Abstract
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.