MiR‑3147 serves as an oncomiR in vulvar squamous cell cancer via Smad4 suppression.

Abstract

The incidence of vulvar squamous cell carcinoma (VSCC) has increased annually over the last decade. MicroRNAs (miRNAs/miRs) serve an important role in tumor progression and development. Our previous microarray studies have revealed that miR-3147 was overexpressed in VSCC. However, its function and underlying mechanism in VSCC remain unknown. In the present study, it was confirmed by reverse transcription-quantitative polymerase chain reaction that the expression of miR-3147 was markedly upregulated in VSCC tissues. The increased expression of miR-3147 was positively associated with the depth of invasion. The overexpression of miR-3147 resulted in the promotion of vulvar cancer cell proliferation, migration, invasion, G1/S progression and invasion-associated gene expression. miR-3147 may participate in the process of epithelial-mesenchymal transition and reduce the expressions of downstream target genes in the transforming growth factor-β/Smad signaling pathway in A431 cells. The knockdown of Smad4 by small interfering RNA promoted malignant behaviours in A431 cells. In addition, miR-3147 regulated Smad4 by directly binding to its 3′ untranslated region. In conclusion, the results indicated that miR-3147 may serve an oncogenic role in VSCC by targeting Smad4. miR-3147 may represent a novel potential therapeutic target marker for VSCC.