LAUSR

Laryngeal carcinoma represents one of the most common types of tumor of the respiratory tract. The aim of the present study was to evaluate the functions of myosin-binding protein C1 (MYBPC1) in the progression of laryngeal carcinoma and to unravel the potential underlying molecular mechanism(s). Significantly differentially expressed mRNAs and miRNAs were analyzed, and potential genes were verified using clinically recruited patients with laryngeal carcinoma. The human laryngeal carcinoma cell lines TU686, TU212 and AMC-HN-8, as well as the control nasopharyngeal epithelial cell line NP69, were selected for the functional analysis of MYBPC1. The interaction between MYBPC1 and miR-451a was also explored in depth. The functions of MYBPC1 in the laryngeal carcinoma cell lines were examined using colony formation assay, cell proliferation and invasion assays, and via measuring the extent of apoptosis. The intracellular function of MYBPC1 was subsequently confirmed by constructing an in vivo xenograft model through the subcutaneous injection of laryngeal carcinoma cells into 4-week-old male nude mice. Compared with normal tissue, MYBPC1 was found to be the most significantly downregulated gene, whereas activating transcription factor-2 (ATF-2) was the most significantly upregulated one. At the same time, miR-451a was found to be the most significantly downregulated miRNA in laryngeal squamous cell carcinoma tissues. According to the WHO classification system, we found that the level of MYBPC1 was significantly decreased in grade IV tissues compared with grade II and grade III tissues, a finding that was consistent with the observed activity of miR-451a. MiR-451a was found to cause a marked enhancement of the activity of MYBPC1 in TU212 cells, which in turn was attenuated by ATF overexpression, suggesting that miR-451a could indirectly modulate the function of MYBPC1 through the ATF2-dependent signaling axis. MYBPC1 suppressed the invasion of cells induced by ATF2 in laryngeal carcinoma cells. Moreover, subcutaneous injection of MYBPC1 to construct an in vivo xenograft mouse model enabled rescue of the mice from laryngeal carcinoma formation. Taken together, the results of the present study have shown that MYBPC1 fulfills a pivotal role in laryngeal carcinoma formation, and these findings may provide both a new avenue for research planning and a potential therapeutic target for laryngeal carcinoma.