PRL‐3 promotes migration and invasion and is associated with poor prognosis in salivary adenoid cystic carcinoma

Background PRL‐3 had been found to be involved in tumorigenesis in various malignancies. In this study, we investigated the role of PRL‐3 in the development, migration, and invasion of salivary adenoid cystic carcinoma (SACC). Methods Immunohistochemistry (IHC) was used to analyze the role of PRL‐3 in the development and prognosis of SACC. Then, we overexpressed or inhibited the expression of PRL‐3 in paired SACC cells to analyze the role of PRL‐3 in the migration and invasion of SACC. In vitro migration and invasion assays were used. Western blotting was used to detect metastasis‐related protein levels. Results IHC results confirmed that the deregulation of PRL‐3 was a frequent event in SACC; the upregulation of PRL‐3 was related to clinical stages, vital status, and distant metastasis, which was associated with reduced overall survival and disease‐free survival. SACC‐LM cells with higher migratory and invasive abilities had more robust PRL‐3 protein expression than SACC‐83 cells with lower migratory and invasive abilities. PRL‐3 overexpression promoted cell migration, invasion, and proliferation, led to simultaneous upregulation of phosphorylated PRL‐3, pERK1/2, Slug, vimentin, and downregulation of E‐cadherin in SACC‐83 cells. However, the inhibition of PRL‐3 by PRL‐3 inhibitor or PRL‐3 siRNA in SACC‐LM cells inhibited cell migration, invasion, and proliferation, resulted in simultaneous downregulation of phosphorylated PRL‐3, pERK1/2, Slug, vimentin, and upregulation of E‐cadherin. Conclusions Our results confirm that PRL‐3 plays an important role in the development of SACC and contributes to the migratory and invasive abilities of SACC.