Small interfering-high mobility group A2 attenuates epithelial-mesenchymal transition in thymic cancer cells via the Wnt/β-catenin pathway

Thymus carcinoma is one of the thymic epithelial neoplasms with high metastasis, which does not have any good treatment at present. High mobility group A2 (HMGA2) is highly expressed in a variety of malignant tumors, such as lung cancer, colon cancer and ovarian cancer and is closely related to tumor invasion and metastasis. The present study aimed to investigate the effect and mechanism of HMGA2 on epithelial-mesenchymal transition (EMT) in thymic cancer cells. IU-TAB-1, A549, HCT-116 and 293T cells were screened by testing the protein expression level of HMGA2 though western blotting and subjected to HMGA2 interference [small interfering (si)-HMGA2]. Cell proliferation was evaluated using the Cell Counting Kit-8 assay. Cell migration and invasion were detected using the Transwell assay. Cell apoptosis was examined using flow cytometry and beta-catenin expression was observed by immunofluorescence. The levels of E-cadherin, vimentin, Wnt3a, Wnt5a and beta-catenin proteins were determined by western blotting. Among the four cell lines tested, IU-TAB-1 cells demonstrated the highest expression of HMGA2 (P<0.05) and were hence selected for subsequent experiments. Compared with the control group (untransfected cells), si-HMGA2 resulted in significantly decreased proliferation, migration and invasion of IU-TAB-1 cells, whereas apoptosis was increased (P<0.05). The protein expression of vimentin, Wnt3a, Wnt5a and beta-catenin was significantly decreased by si-HMGA2 compared with the control group (P<0.05), whereas E-cadherin expression was increased (P<0.05). After treatment with si-HMGA2 in combination with Wnt/beta-catenin agonists (SKL2001) or inhibitors (XAV-939), EMT was respectively enhanced or inhibited in IU-TAB-1 cells. Overall, si-HMGA2 may attenuate EMT in thymic cancer cells and the mechanism may be related to the Wnt/beta-catenin pathway.

Automated summary

The study investigated the impact of HMGA2 on epithelial-mesenchymal transition (EMT) in thymic cancer cells, suggesting that si-HMGA2 may regulate EMT via the Wnt/β-catenin pathway.