Abstract
Anaplastic thyroid cancer (ATC), with a mean survival time of 6 months, was reported in 2012 to account for 1-2% of all thyroid tumor cases in the US. Understanding the molecular mechanisms underlying carcinogenesis and progression in ATC would contribute to determining novel therapeutic targets. The aberrant expression of microRNA-544 (miR-544) has been demonstrated in various cancer types. However, its expression and biological function in human ATC remain largely unknown. Therefore, the present study investigated the expression, function and molecular mechanism of miR-544 in ATC. Results of reverse transcription-quantitative polymerase chain reaction demonstrated that the expression levels of miR-544 in 40 pairs of surgical specimens and human ATC cell lines were significantly decreased, compared with the normal thyroid tissues and cell line. Functional assays indicated that ectopic expression of miR-544 significantly decreased the viability, proliferation and metastasis of SW1736 cells, whereas miR-544 inhibitor significantly enhanced the viability, proliferation and metastasis of 8305C cells. Furthermore, the present study confirmed that the oncogene Yin Yang-1 (YY1) was a direct target of miR-544. It was further demonstrated that YY1 overexpression rescued the inhibitory effect of progression induced by miR-544 in ATC cells. Finally, in vivo study indicated that miR-544 suppressed the tumorigenicity of ATC cells. In conclusion, the present study demonstrated that miR-544 may function as a tumor suppressor in ATC and serve as a future therapeutic target for patients with ATC.