Colorectal cancer (CRC) was one of the most malignant tumors worldwide due to its metastasis. Epithelial-to-mesenchymal transition (EMT) plays an important role in CRC migration, and transforming growth factor-β (TGF-β) works as a dominating cytokine in CRC EMT process. Here, we originally identified RUNX1 as an important factor among TGF-β induced EMT in CRC. We found that RUNX1 was overexpressed with the treatment of TGF-β, accompanied with enhanced cancer cell migration and EMT which was characterized by up-graded N-Cadherin levels. Vice versa, knockdown of RUNX1 attenuated the migration ability of TGF-β induced CRC cells. In addition, decreased expression of N-Cadherin suggested that EMT was also attenuated after knocking down RUNX1. Similar decrease was observed in EMT regulator snail family transcriptional repressor 1 (SNAI1). And the knockdown effect of RUNX1 cannot be reversed by the addition of TGF-β. Moreover, we observed that RUNX1 expression was higher in CRC tumor tissues than in normal epithelial tissues. The enhanced expression was detected in cancer cell nucleus. These results revealed RUNX1 could regulate colorectal cancer migration via TGF-β signaling pathway, and RUNX1 might serve as a potential target for preventing CRC metastasis.
Keywords: EMT; RUNX1; TGF-β; colorectal cancer; metastasis.
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