RASSF10 exhibits tumor-suppressing potential involving tumor proliferation, metastasis and epithelial-mesenchymal transition in esophageal squamous cell carcinoma

Growing evidence indicates that Ras-association domain family 10 (RASSF10) is a novel tumor-suppressor gene that is involved in the inhibition of tumor progression and metastasis; however, the biological functions and molecular mechanisms of RASSF10 in esophageal squamous cell carcinoma (ESCC) have not yet been thoroughly elucidated. The expression of RASSF10 in ESCC tissues and adjacent non-tumor tissues was investigated employing quantitative polymerase chain reaction (qPCR) and immunohistochemistry (IHC) assays of tissue microarrays. The function of RASSF10 in ESCC cell growth, migration and invasion was determined by CCK-8, colony formation, scratch wound healing and Transwell invasion assays, respectively. The correlation between RASSF10 and markers related to epithelial-mesenchymal transition (EMT) was evaluated by tissue microarray (TMA)-IHC, western blotting and immunofluorescence staining. RASSF10 was found to be highly downregulated in ESCC tissues compared with that noted in the adjacent non-tumor tissues, and closely correlated with tumor progression and patient prognosis. Moreover, functional studies demonstrated that RASSF10 overexpression not only resulted in reduced cell growth and colony formation but also inhibited migration and invasion of the ESCC cells. Tumor RASSF10 expression was positively correlated with E-cadherin expression and negatively correlated with vimentin. In addition, it was demonstrated that the antineoplastic functions of RASSF10 mediate inactivation of the Wnt/beta-catenin pathway in ESCC. Our findings revealed that RASSF10 may constitute a prognostic factor for ESCC patients and a crucial candidate for targeted therapy against ESCC.