PLK1 gene suppresses cell invasion of undifferentiated thyroid carcinoma through the inhibition of CD44v6, MMP-2 and MMP-9

The aim of this study was to observe the regulatory action of the polo-like kinase 1 (PLK1) gene in the invasion of anaplastic thyroid carcinoma cells and investigate its mechanisms. The expression of the PLK1 protein in 36 patients with anaplastic thyroid carcinoma was detected by immunohistochemical staining. siRNA against PLK1 was designed, synthesized and transfected into ARO cells. The effects of PLK1 siRNA on cell invasion were detected by a soft agar colony formation assay and a Transwell chamber assay. The corresponding protein was detected using western blot analysis. The expression of PLK1 in anaplastic thyroid carcinoma samples (67.5±10.6%) was significantly higher compared to that in cancer-adjacent samples (0.65%±0.12%; P<0.01). The expression of PLK1 correlated with clinical stage, lymph node metastasis and prognosis of anaplastic thyroid. The number of cell clones was reduced in a dose-dependent manner with increasing levels of siRNA and the number of cells permeating through the filter membrane decreased following transfection with siRNA. The inhibition of PLK1 caused a significant decrease in CD44v6, matrix metalloproteinase (MMP)-2 and MMP-9 (0.36±0.08, 0.12±0.03, 0.25±0.06, respectively) compared to the non-transfected group (1.15±0.18, 1.21±0.20, 1.25±0.21, respectively; P<0.01). In conclusion, the expression of PLK1 was found to be increased in anaplastic thyroid carcinoma and was correlated with clinical stage, lymph node metastasis and prognosis. Additionaly, PLK1 siRNA was found to inhibit the invasion of anaplastic thyroid carcinoma cells. Therefore, CD44v6, MMP-2 and MMP-9 are likely to be involved in the regulation of cell invasion induced by PLK1.