HMGA2 promotes epithelial-mesenchymal transition of clear cell renal cell carcinoma via transforming growth TGF-β/Smad2 signal pathways

Abstract

Abstract Purpose To investigate the role of high mobility group protein A2 (HMGA2) in the epithelial-mesenchymal transition (EMT) of kidney cancer. Methods The renal carcinoma cell line ACHN were transfected using RNA interference technology (siRNA) to develop a cell line with low HMGA2 expression. The expression of E-cadherin, N-cadherin, and zinc finger protein (Snail) was detected using quantitative real-time polymerase chain reaction and Western blot at the mRNA and protein levels. Results The results show that the mechanism of HMGA2 action on kidney cancer cells is related to EMT, and this action is achieved by influencing the EMT marker proteins E-cadherin and N-cadherin. The mechanism where HMGA2 exerts its biological function is related to the transforming growth factor-β (TGF-β) signaling pathway, where HMGA2 is able to interact with Smad2 and Smad3. In the TGF-β signaling pathway, HMGA2 can bind and form a complex with Smad2 and Smad3 to induce the expression of the target gene, Snail, promote the production of Snail protein, and induce EMT in kidney cancer cells, thereby promoting the occurrence and development and metastasis of kidney cancer cells. Conclusion HMGA2 is closely related to the migration and invasive ability of kidney cancer cells and can promote EMT of kidney cancer cells by activating the intracellular TGF-β signaling pathway. In kidney cancer cells, the intracellular TGF-signaling pathway promotes EMT.