miR-204 enhances p27 mRNA stability by targeting Brd4 in head and neck squamous cell carcinoma.

The present study aimed to explore the function of microRNA (miR)-204 in modulating cyclin-dependent kinase inhibitor 1B (p27) mRNA stability in head and neck squamous cell carcinoma (HNSCC). Briefly, reverse transcription quantitative polymerase chain reaction and western blot analysis were used to detect miR-204 and Brd4 level. Cell viability, cell cycle and cell apoptosis were used to investigate the effects of miR-204. Additional luciferase reporter and mRNA stability assays were used to explore the mechanisms contributing to miR-204 effects. Here, miR-204 was downregulated in HNSCC tissues compared with the adjacent normal tissues. The expression levels of miR-204 and bromodomain-containing protein 4 (Brd4) were negatively associated in HNSCC tissues. Ectopic expression of miR-204 inhibited HNSCC cell proliferation, promoted cell cycle arrest at the G1/S phase and promoted cell apoptosis compared with control cells. Additionally, upregulation of miR-204 expression levels enhanced p27 mRNA stability. Notably, Brd4 was identified as a target of miR-204, and the co-expression of Brd4 with miR-204 mimics attenuated the inhibitory effects of miR-204 on cell proliferation and enhanced p27 mRNA stability compared with control cells. Thus, it was concluded that miR-204 functions as a tumor suppressor by enhancing p27 mRNA stability through targeting Brd4 in HNSCC.