MiR-24 functions as a tumor suppressor in nasopharyngeal carcinoma through targeting FSCN1

Background: increasing evidence indicates that the dysregulation of mirnas expression is involved in the tumorigenesis by acting as tumor suppressors or oncogenes. however,no study investigates the function and mechanisms of mir-24 in nasopharyngeal carcinoma (npc). methods: quantitative rt-pcr,mtt,colony formation,soft-agar,wound healing,transwell migration and invasion assays,and xenograft tumor growth and lung metastasis models were performed to test the expression levels and functions of mir-24 in npc. luciferase reporter assay,quantitative rt-pcr,western blotting,and immunohistochemistry were used to identify and verify the target of mir-24. results: the results showed that mir-24 was obviously downregulated in npc cell lines and tissue samples (p∈<∈0.05). ectopic expression of mir-24 inhibited the cell viability,proliferation,migration,and invasion in vitro (all p∈<∈0.05),and suppressed the xenograft tumor growth and lung metastasis formation in vivo (all p∈<∈0.05). fascin homologue 1 (fscn1) was verified as a direct target of mir-24,and silencing fscn1 expression with small interfering rna inhibited npc cell proliferation and invasion (all p∈<∈0.05). conclusions: overall,mir-24 acts as a novel tumor suppressor in the development and progression of npc through targeting fscn1,which providing new insight into the mechanisms of npc carcinogenesis and suggesting the possibility of mir-24 as a therapeutic target. © 2015 li et al.