Silencing NEAT1 suppresses thyroid carcinoma via miR-126/NEAT1/VEGFA axis.

The incidence of papillary thyroid carcinoma (PTC) has steadily increased over the recent years, making this cancer a common malignant tumor world-wide. We tested the hypothesis that Nuclear Enriched Abundant sh-NEAT1 knock-down ranscript 1 (NEAT1) is involved in the pathogenesis of PTC in vitro and in vivo. We show that NEAT1 is highly expressed in Papillary Thyroid Carcinoma cell line (PTC-1) and anaplastic thyroid cancer cell line (SW1736) as compared with the human thyroid follicular epithelial cell line (Nthy-ori 3-1). shRNA knockdown of NEAT1 led to the inhibition of cell growth, invasion, migration and Epithelial to Mesenchymal Transition (EMT) of thyroid cancer cells. This treatment increased the rate of apoptosis in SW1736 cells. Silencing of NEAT1 increased the level of its regulator, miRNA-126 and down-regulated VEGFA that sets the density of tumor vasculature. Administrtation of sh-NEAT1 also inhibited tumor growth in vivo, increased the miRNA-126 level and down-regulated VEGFA. Taken together, these results indicate that silencing NEAT1 suppresses thyroid carcinoma via miR-126/NEAT1/VEGFA axis.