Study on miR-29a inhibiting papillary thyroid carcinoma by downregulating TAGLN2

This study aims to explore the possible mechanism of miR-29a inhibiting papillary thyroid carcinoma (PTC) through the downregulation of TAGLN2. The paper expects to find novel targets for PTC treatment and prognosis improvement, and is also of great significance in enhancing the overall therapeutic level of PTC and improving life quality of patients. Changes in PTC cell growth, migration, and invasive ability were respectively detected using MTS assays, wound healing experiments, and Matrigel matrix invasion assays. Expressions of E-cadherin, N-cadherin, vimentin, and MMP2 were determined by Western blotting. Differences in protein expressions between groups were compared. Overexpression and knockdown of TAGLN2 were performed in K1 cells, and the expression levels of PI3K/AKT pathway protein in K1 cells were detected by Western blotting. miR-29a significantly inhibited the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of K1 cells. Overexpression of miR-29a played an important role in improving the malignant phenotype of PTC by regulating the expression of actin-binding protein TAGLN2. Overexpression of TAGLN2 can counteract the inhibitory effect of miR-29a on K1 cells. TAGLN2 can activate the PI3K/AKT signaling pathway, indicating that it may promote the progress of EMT by activating PI3K/AKT. The miR-29a/TAGLN2 axis may affect the malignant phenotype of K1 cells by regulating downstream PI3K/AKT signaling pathways, thus providing a new target for the treatment of PTC.