D-K Liu1, S Yu, J-P Li, W-W Song, J-H Li. 1. Department of Stomatology, Yantaishan Hospital, Yantai, China. quydtotr508855@163.com.
Abstract
OBJECTIVE: Oral squamous cell carcinoma (OSCC) accounts for 90% of head and neck cancers, and its 5-year overall survival is very poor. MiR-150 is usually downregulated and acts as tumor suppressor in multiple cancers. The aim of our study is to explore the functions of miR-150 in OSCC. PATIENTS AND METHODS: Expressions of miR-150 and HMGA2 mRNA in OSCC tissues and cells were analyzed by qRT-PCR. Methyl Thiazolyl Tetrazolium (MTT) and transwell assays were conducted to assess the cell viability and invasive abilities. Western blot was conducted to assess the protein levels of epithelial-mesenchymal transition (EMT) markers. Luciferase reporter assay was carried out to verify miR-150 directly binding to HMGA2 in SCC25 cells. RESULTS: MiR-150 was low expressed and HMGA2 was highly expressed in OSCC tissues and cells. Downregulation of miR-150 or upregulation of HMGA2 predicted poor prognosis of OSCC patients. MiR-150 overexpression inhibited the abilities of viability, invasive and the EMT by targeting HMGA2 in OSCC cells. HMGA2 was a target gene of miR-150 and its expression was regulated by altering the expression of miR-150 in OSCC cells. HMGA2 reversed partial roles of miR-150 on cell viability and invasion in OSCC. CONCLUSIONS: MiR-150 impaired cell viability, invasion and EMT via binding to HMGA2 of OSCC. Our research demonstrates that miR-150 plays a critical role in the progression of OSCC. miR-150 might be a candidate molecular marker and a novel therapy target for OSCC patients.
OBJECTIVE: Oral squamous cell carcinoma (OSCC) accounts for 90% of head and neck cancers, and its 5-year overall survival is very poor. MiR-150 is usually downregulated and acts as tumor suppressor in multiple cancers. The aim of our study is to explore the functions of miR-150 in OSCC. PATIENTS AND METHODS: Expressions of miR-150 and HMGA2 mRNA in OSCC tissues and cells were analyzed by qRT-PCR. Methyl Thiazolyl Tetrazolium (MTT) and transwell assays were conducted to assess the cell viability and invasive abilities. Western blot was conducted to assess the protein levels of epithelial-mesenchymal transition (EMT) markers. Luciferase reporter assay was carried out to verify miR-150 directly binding to HMGA2 in SCC25 cells. RESULTS: MiR-150 was low expressed and HMGA2 was highly expressed in OSCC tissues and cells. Downregulation of miR-150 or upregulation of HMGA2 predicted poor prognosis of OSCC patients. MiR-150 overexpression inhibited the abilities of viability, invasive and the EMT by targeting HMGA2 in OSCC cells. HMGA2 was a target gene of miR-150 and its expression was regulated by altering the expression of miR-150 in OSCC cells. HMGA2 reversed partial roles of miR-150 on cell viability and invasion in OSCC. CONCLUSIONS: MiR-150 impaired cell viability, invasion and EMT via binding to HMGA2 of OSCC. Our research demonstrates that miR-150 plays a critical role in the progression of OSCC. miR-150 might be a candidate molecular marker and a novel therapy target for OSCC patients.