부산대학교 도서관

Purpose: SOX12 is overexpressed in many cancers, and we aimed to explore the biological function and mechanism of SOX12 inthyroid cancer. Materials and Methods: We first analyzed the expression of SOX12 in thyroid cancer using data in The Cancer Genome Atlas. Immunohistochemistryand qRT-PCR were performed to identify SOX12 expression in thyroid cancer tissue and cells. Thyroid cancercells were transfected with small interfering RNA targeting SOX12, and cellular functional experiments, including CCK8, woundhealing, and Transwell assays, were performed. Protein expression was examined by Western blot analysis. A xenograft model wasdeveloped to evaluate the effect of SOX12 on tumor growth in vivo. Results: SOX12 expression was increased in thyroid cancer tissue and cells. SOX12 promoted cell proliferation, migration, and invasionand accelerated tumor growth in vivo. The expression of PCNA, Cyclin D1, E-cadherin, Snail, MMP-2, and MMP-9 was affectedby SOX12 knockdown. Bioinformatic analysis showed that SOX12 could interact with the POU family. SOX12 knockdown inhibitedthe expression of POU2F1, POU2F2, POU3F1 and POU3F2, and SOX12 expression showed a positive correlation with POU2F1,POU3F1, and POU3F2 expression in clinical data. POU2F1 and POU3F1 were able to reverse the effect of SOX12 knockdown onthyroid cancer cells. Conclusion: SOX12 affects the progression of thyroid cancer by regulating epithelial-mesenchymal transition and interacting withPOU2F1 and POU3F1, which may be novel targets for thyroid cancer molecular therapy.