MicroRNA­195 is associated with regulating the pathophysiologic process of human laryngeal squamous cell carcinoma.

ABSTRACT

MicroRNAs (miRNAs) have been reported to be associated with the modulation of tumor development, including alterations associated with the development of human laryngeal squamous cell carcinoma (LSCC). The present study was designed to investigate whether miRNA­195 was associated with the pathophysiologic process of human LSCC and to identify its potential roles and underlying molecular mechanisms. To determine whether miRNA­195 serves a role in LSCC, reverse transcription­quantitative polymerase chain reaction was used to detect miRNA­195 expression in LSCC tissues. The tumor­suppressive effect of miRNA­195 was determined by in vitro assays. Gain­of­function studies using miRNA­195 mimics were performed to investigate cell viability, migration and invasion, and apoptosis in the AMC­HN­8 cell line. Western blotting was performed to reveal the molecular mechanisms of miRNA­195 and its downstream signaling pathways in the LSCC AMC­HN­8 cell line. The present study demonstrated that miRNA­195 is downregulated in primary LSCC tumors. Upregulating miRNA­195 in vitro suppressed cell viability, migration and invasion in AMC­HN­8 cells. Overexpression of miRNA­195 alone in AMC­HN­8 cells was sufficient to induce cell apoptosis, as identified by terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Compared with the high expression of miRNA­195 in AMC­HN­8 cells, the expression levels of vascular endothelial growth factor receptor­II protein and downstream signaling pathway proteins, which were associated with cell viability, migration, invasion and apoptosis, were markedly decreased compared with control or miRNA­195 negative control treatment group. Together, these data suggest the therapeutic potential of miRNA­195 in modulating cell growth, migration and apoptosis during the pathophysiological progression of LSCC and that miRNA­195 may serve as a potential therapeutic target in human LSCC.