Abstract
MicroRNA (miR)‑26a‑5p and miR‑26b‑5p consistently play an antitumor role in many types of cancers, but the underlying mechanism remains unclear in bladder cancer (BC). In the present study, we found that, in BC tissues, the levels of miR‑26a‑5p and miR‑26b‑5p were lower than in paired normal tissues. The upregulation of miR‑26‑5p significantly inhibited the proliferation of BC cell lines (T24 and 5637). Bioinformatics analysis indicated that Programmed Cell Death 10 (PDCD10) was the downstream target gene of miR‑26a‑5p/miR‑26b‑5p, and this was ascertained by western blotting and quantitative real‑time reverse transcription PCR (RT‑qPCR). In addition, in the 3'‑UTR of PDCD10, the binding site was identified using a luciferase reporter assay. We determined that clinical BC tissues presented higher PDCD10 levels than adjacent normal tissues and that PDCD10 promoted proliferation of BC cell lines. Overexpression of miR‑26a‑5p/miR‑26b‑5p inhibited the stimulatory effect on proliferation of BC cells induced by PDCD10. In addition, in vivo experiments and clinical data revealed that the prognosis of BC patients with high expression of miR‑26a‑5p/miR‑26b‑5p and low expression of PDCD10 was better than that of patients with low miR‑26‑5p and high PDCD10 expression. These data revealed that miR‑26a‑5p and miR‑26b‑5p were pivotal regulators in BC progression by targeting the proliferation‑related protein, PDCD10. The miR‑26‑5p/PDCD10 interaction may provide important insight into the pathway of BC progression and present novel opportunities for future diagnosis and treatment strategies, especially for patients with high levels of PDCD10.