Abstract
Salivary adenoid cystic carcinoma (SACC) exhibits slow continuous growth, frequent local recurrences and a high incidence of blood metastasis, with advanced lung metastasis frequently occurring and being among the primary causes of mortality. MicroRNAs (miR) serve a significant role in the initiation and development of cancer and may be tumour‑specific molecular targets. However, the role of miR‑103a‑3p in SACC remains largely unknown. In the present study, the expression levels of miR‑103a‑3p and tumour protein D52 (TPD52) were detected by reverse transcription‑quantitative PCR. In addition, wound‑healing assays, Transwell assays and mouse models of lung metastasis were used to investigate the biological functions exerted by miR‑103a‑3p. The present results suggested that miR‑103a‑3p expression was significantly upregulated in SACC samples. Gain‑of‑function and loss‑of‑function studies in SACC cells demonstrated that miR‑103a‑3p acted as an oncogene by promoting tumour cell migration in vitro and lung metastasis in vivo. Dual‑luciferase reporter gene assays indicated that miR‑103a‑3p exerted its regulatory functions by binding to the 3' untranslated region of TPD52 mRNA. TPD52 overexpression rescued the effect of miR‑103a‑3p on promoting SACC cell migration, suggesting that miR‑103a‑3p acted as an oncogene to promote cancer metastasis by directly targeting TPD52. Thus, the newly identified miR‑103a‑3p/TPD52 axis contributes to the understanding of SACC pathogenesis, providing insights into the identification of novel biomarkers or potential therapeutic targets in SACC.