MiR-29b suppresses proliferation and mobility by targeting SOX12 and DNMT3b in pancreatic cancer.

Pancreatic cancer is one of the leading causes of solid carcinoma with the worst survival rate. The reasons for the worst survival rate include the lack of biomarkers for early detection, diagnosis at a late stage, and the limitation of the current therapy. Further study to investigate the underlying molecular mechanism in pancreatic cancer patients is necessary. A previous study showed that the miR-29b expression level is dysregulated, suggesting that it may serve an important function in pancreatic cancer. The CCK8 assay and the colony formation assay were used to detect the proliferation ability of the treated pancreatic cancer cells; a wound-healing assay and a transwell assay were used to test the migration and invasion ability and the interactive action of miR-29b and SOX12 or DNMT3b was examined by a luciferase assay. Cell proliferation, migration, and invasion were attenuated by miR-29b, whereas knockdown of SOX12 and DNMT3b could block SW1990 malignant activity. Further, the double luciferase assay showed that miR-29b can target SOX12 and DNMT3b directly by binding to their 3'-untranslated region. Finally, a rescue experiment was conducted by transfecting miR-29b and SOX12 overexpressed plasmid into cells. Cell proliferation, migration, and invasion inhibition induced by miR-29b were reversed by SOX12 overexpression, and revail of the expression of DNMT3b. MiR-29b suppressed proliferation, migration, and invasion by directly targeting SOX12 and DNMT3b in pancreatic cancer cells, and DNMT3b might be a target gene of SOX12.