Abstract

Tongue squamous cell carcinoma (TSCC) is the most frequently occurring oral cancer and is characterized by high proliferation and metastasis rates. Incomplete understanding of the pathogenesis of TSCC coupled with frequent tongue movement increases the difficulty of therapy. Additionally, TSCC is prone to recurrence and metastasis after treatment. Thus, exploring mechanisms of proliferation, migration, and infiltration of TSCC cancer cells is essential for reducing morbidity and mortality. Transfection of miRNA-200a mimics into SCC15 cells showed that miRNA-200a expression decreased significantly, and DEK expression significantly increased. Transfection of miRNA-200a mimics (miRNA-200a group), negative control mimics (miRNA-NC group), empty vector (miRNA-200a + pcDNA3.1 group), and miRNA-200a mimics and DEK overexpression vector (miRNA-200a + DEK group) into SCC15 cells respectively indicates that overexpression of miRNA-200a substantially inhibits SCC15 cell proliferation, infiltration and migration, decreases PCNA and Vimentin expression, and promotes E-cadherin expression. miRNA-200a + DEK transfection induced greater cell proliferation, infiltration and migration, much higher PCNA and Vimentin expression, and significantly lower E-cadherin expression. Luciferase reporter gene detection of overexpressed DEK or DEK expression after inhibiting miRNA-200a expression indicated a targeting association between miRNA-200a and DEK. miRNA-200a inhibits proliferation, infiltration and migration ability of TSCC by targeting DEK and may represent a novel means for clinical intervention in TSCC. miRNA-200a inhibits proliferation, invasion, and migration of TSCC by targeting DEK.

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