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miR-206 inhibits human laryngeal squamous cell carcinoma cell growth by regulation of cyclinD2.

Authors :
Yu WF
Wang HM
Lu BC
Zhang GZ
Ma HM
Wu ZY
Source :
European review for medical and pharmacological sciences [Eur Rev Med Pharmacol Sci] 2015; Vol. 19 (14), pp. 2697-702.
Publication Year :
2015

Abstract

Objective: Accumulating evidence has shown that microRNAs (miRNAs) are aberrantly expressd in many malignancies and crucial to tumorigenesis. Herein, we identified the role and mechanism of miR-206 in laryngeal squamous cell carcinoma (LSCC) growth.<br />Patients and Methods: Quantitative real-time PCR was performed to detect the relative expression level of miR-206 in LSCC tissues. Crystal violet and flow cytometry were conducted to explore the effects of miR-206 on the proliferation and cell cycle of human LSCC cell line, respectively. The impact of miR-206 overexpression on putative target cyclinD2 were subsequently verified via Western blot. Tumor growth assay was performed to testify the effect of miR-206 on the tumor growth in vivo.<br />Results: MiR-206 expression was frequently (p < 0.05) down-regulated in LSCC specimens. Overexpression of miR-206 in Hep-2 cell inhibited the proliferation by blocking the G1/S transition as well as suppressed the growth of xenograft tumors in mice, implying that miR-206 functions as a tumour suppressor in the progression of LSCC. Overexpression of miR-206 significantly decreased (p < 0.05) the protein level of cyclinD2, which has previously been identified as a direct targets of miR-206.<br />Conclusions: Altogether, our results identify a crucial tumour suppressive role of miR-206 in LSCC growth, at least partly via up-regulation of cyclinD2 protein levels, and suggest that miR-206 might be a candidate prognostic predictor or an anticancer therapeutic target for LSCC patients.

Details

Language :
English
ISSN :
2284-0729
Volume :
19
Issue :
14
Database :
MEDLINE
Journal :
European review for medical and pharmacological sciences
Publication Type :
Academic Journal
Accession number :
26221902