Proinflammatory factor tumor necrosis factor-α (TNF-α) is an important inflammatory mediators in tumor microenvironment and autoimmune diseases, it is highly expressed in many solid tumors and tumor microenvironment, showing a tumor promoting role. However, the molecular mechanisms underlying TNF-α-increased invasion of thyroid cancer are still not fully understood. In order to explore whether TNF-α plays a key role in the process of epithelial mesenchymal transition (EMT) in papillary thyroid carcinoma (PTC), we used TNF-α to induce EMT in different PTC cell lines, and observed the expression of different transcription factors and signal pathways. After TNF-α treatment, in TPC-1, Snail and ZEB2 mRNA levels did not change significantly, while Slug, Twist1, ZEB1 mRNA expression increased. In BCPAP, Snail mRNA level increased significantly (P < 0.01), while Twist1 showed a certain degree of increase only at the concentration of TNF - α 20 ng / ml (P < 0.01), but mRNA of Slug, ZEB1, ZEB2 showed no significant change. The expression of proteins was consistent with genes. The activation of different pathways did not show gene differences, and pathway inhibitors could reduce the invasion and metastasis of cells, but only NF-κB inhibitors could reverse the expression of transcription factors. Expressions of Snail and Slug in different PTC cell lines were dependent on pro-oncogene mutation, but the pathway had no differences. The establishment of this study model can enrich the research on the pathogenesis and metastasis of thyroid cancer, effectively link the inflammatory microenvironment with the occurrence and development of thyroid cancer.
Keywords: EMT; NF-κB; PTC; TNF-α; transcription factors..
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