MicroRNA‑16‑5p/BIMP1/NF‑κB axis regulates autophagy to exert a tumor‑suppressive effect on bladder cancer.

Bladder cancer (BC) is the second most common urological disease worldwide. Previous studies have reported that microRNA (miR)‑16‑5p is associated with the development of BC, but whether miR‑16‑5p regulates BC cell autophagy remains unknown. Thus, the aim of the present study was to investigate this issue. miR‑16‑5p expression in BC cells was assessed by reverse transcription‑quantitative PCR. Cell viability and apoptosis were detected via Cell Counting Kit‑8 and flow cytometry assays, respectively. For cell autophagy detection, autophagic flux was detected using a mCherry‑green fluorescent protein‑microtubule‑associated proteins 1A/1B light chain 3B (LC3) puncta formation assay, followed by determination of autophagy‑related protein markers. The targeting relationship between miR‑16‑5p and caspase recruitment domain family member 10 (BIMP1) was confirmed using a dual‑luciferase reporter assay, followed by detection of the BIMP1/NF‑κB signaling pathway. The results showed that miR‑16‑5p overexpression inhibited cell viability, whereas miR‑16‑5p knockdown promoted cell viability in BC. Furthermore, miR‑16‑5p overexpression induced autophagy, which was accompanied by increased autophagic flux and expression of the autophagy‑related proteins LC3‑II and beclin 1, as well as decreased p62 expression, whereas miR‑16‑5p silencing led to an inhibition of autophagy in BC cells. Moreover, autophagy inhibitor 3‑methyladenine treatment inhibited cell autophagy and apoptosis in miR‑16‑5p‑overexpressing cells. Mechanistic studies demonstrated that miR‑16‑5p could inhibit the BIMP1/NF‑κB signaling pathway and this inhibition was achieved by directly targeting BIMP1. Furthermore, it was found that blockade of the BIMP1/NF‑κB signaling pathway inversed the inhibitory effects of miR‑16‑5p knockdown on autophagy in BC cells.