MiR-155 is overexpressed in different types of tumors, including colon cancer. High expression of miR-155 has been correlated with poor prognosis in colorectal cancer patients suggesting a pro-carcinogeneic role of miR-155. Increased RNA translation induced by miRNAs has been shown to be mediated via AU-rich elements (AREs) in the 3′ untranslated region (UTR) of mRNA for instance AUUA and AUUUA, as well as adjoining non-AU sequences. Notably, investigations have reported that miR-155 can regulate migration and invasion of certain tumor cell types, such as breast, colon, pancreatic, hepatocellular and nasopharyngeal cancers. However, the role and mechanism of MiR-155 in regulating chemokine-induced colon cancer cell migration remains poorly understood. HuR has been shown to regulate RhoA, while miR-155 has been recently demonstrated to target directly RhoA in positive regulation manner in serum starved cells. RhoA belongs to a GTPase oncogenic family which has AU rich elements in the 3-UTR region. The regulation was confirmed by direct binding of miR-155-5p to these motifs (Amr A. Al-Haidari, et al. MiR-155-5p positively regulates CCL17-induced colon cancer cell migration by targeting RhoA, Oncotarget. 2017 Feb 28; 8(9): 14887–14896). Interestingly, HuR can bind RhoA in these motifs as well and this could explain at least in part the RhoA regulation by miR-155-5p and why cancer cells exploit this regulation profile in early tumorigenesis phases. In this project, we are trying to understand how HuR contributes to colon cancer metastasis.