targets angiogenesis and EMT concurrently in anaplastic thyroid carcinoma.

The current study aims to evaluate for the first time the inhibitory roles of in the pathogenesis of anaplastic thyroid carcinoma. In addition, we investigated the mechanisms by which miR-205 regulates angiogenesis and epithelial-to-mesenchymal transition (EMT) in cancer. Two anaplastic thyroid carcinoma cell lines were transfected with the expression vector pCMV- Selected markers of angiogenesis and EMT including vascular endothelial growth factor A () and zinc finger E-box-binding homeobox 1 () were investigated by Western blot. The interaction of expression with EMT and angiogenesis were also investigated by assessment of matrix metalloproteinases 2 and 9 (MMP2 and MMP 9), SNAI1 (Snai1 family zinc finger 1), vimentin, E-cadherin and N-cadherin. The function of was further tested with VEGF enzyme-linked immunosorbent assay (ELISA), wound healing, invasion and tube formation assays. Using an animal model, we studied the association of with angiogenesis, proliferation and invasion. The following results were obtained. Permanent overexpression of significantly suppressed angiogenesis and EMT by simultaneously targeting , and downstream products. Ectopic expression of in cancer cells led to decreased migration, invasion and tube formation of endothelial cells. In addition, inhibition of tumour growth, vascularisation and invasion were noted in the mouse tumour xenografts. Our findings provide insights into simultaneous regulatory role of in the pathogenesis of anaplastic thyroid carcinoma by suppressing both angiogenesis and EMT. This may open avenues to exploit as an alternative cancer therapeutic strategy in the future.