// Liang Zhong 1 , Bryan Simoneau 1 , Jacques Huot 1 , Martin J. Simard 1 1 St-Patrick Research Group in Basic Oncology, CHU de Québec-Université Laval Research Centre (Hôtel-Dieu de Québec), Laval University Cancer Research Centre, Quebec City, Québec, G1R 2J6, Canada Correspondence to: Jacques Huot, email: Jacques.Huot@fmed.ulaval.ca Martin J. Simard, email: Martin.Simard@crchudequebec.ulaval.ca Keywords: c-Fos, c-Jun, GATA2, IL-1β metastasis, endothelial cells Received: April 06, 2016 Accepted: October 31, 2016 Published: December 02, 2016 ABSTRACT Extravasation of circulating cancer cells is a key event of metastatic dissemination that is initiated by the adhesion of cancer cells to vascular endothelial cells. It requires the interaction between adhesion receptors such as E-selectin present on endothelial cells and their ligands on cancer cells. Notably, E-selectin influences the metastatic potential of breast, bladder, gastric, pancreatic, and colorectal carcinoma as well as of leukemia and lymphoma. Here, we show that E-selectin expression induced by the pro-inflammatory cytokine IL-1β is directly and negatively regulated by miR-31. The transcription of miR-31 is activated by IL-1β. This activation depends on p38 and JNK MAP kinases, and their downstream transcription factors GATA2, c-Fos and c-Jun. The miR-31-mediated repression of E-selectin impairs the metastatic potential of colon cancer cells by decreasing their adhesion to, and migration through, the endothelium. These results highlight for the first time that microRNA mediates E-selectin-dependent extravasation of colon cancer cells.
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Zhong et al. (2016) studied this question.