MicroRNA‑199a‑5p suppresses migration and invasion in oral squamous cell carcinoma through inhibiting the EMT‑related...

MicroRNAs (miRs) are small, non‑coding RNAs that can act as oncogenes or tumor suppressor genes in human cancer. Recent studies have revealed that miR‑199a‑5p is abnormally expressed in various types of human cancer; however, the potential role of miR‑199a‑5p in oral squamous cell carcinoma (OSCC) remains elusive. The present study investigated the role of miR‑199a‑5p in OSCC cells and explored the potential molecular mechanism. Reverse transcription‑quantitative polymerase chain reaction was used to measure miR‑199a‑5p expression in OSCC tissues and adjacent normal oral epithelial tissues. Cell invasion and migration were evaluated using Transwell invasion and wound‑healing assays in OSCC cells post‑transfection with miR‑199a‑5p mimics or negative control mimics. In addition, a luciferase reporter assay was conducted to identify the target gene of miR‑199a‑5p in OSCC cells. The results demonstrated that miR‑199a‑5p expression was significantly downregulated in OSCC tissues and cell lines, and was associated with tumor progression in OSCC. Furthermore, overexpression of miR‑199a‑5p inhibited cell invasion and migration, and blocked the epithelial‑mesenchymal transition (EMT) cascade. Notably, the results revealed that the EMT‑related transcription factor SRY‑box 4 (SOX4) was a direct target gene of miR‑199a‑5p, as determined by the direct binding of miR‑199a‑5p with the 3'‑untranslated region of SOX4. In addition, knockdown of SOX4 by small interfering RNA‑SOX4 suppressed proliferation, migration and invasion of OSCC cells. Conversely, overexpression of SOX4 rescued the suppressive effects of miR‑199a‑5p on cell migration and invasion. Collectively, these data indicated that miR‑199a‑5p may inhibit the migration and invasion of OSCC cells via targeting the EMT‑related transcription factor SOX4, thus suggesting that miR‑199a‑5p may serve as a prognostic biomarker and therapeutic target in the treatment of OSCC.