This is consistent with evidence showing that the therapeutic inhibition of MALAT1 suppressed the invasion and metastasis of colorectal cancer cells via mediation of the Wnt/β-catenin signaling pathway [30], and that up-regulated MALAT1 in high-fat food fed ApoE−/− mice enhanced the nuclear translocation of β-catenin and activation of Wnt/β-catenin signaling, with associated increase in angiogenesis biomarker CD31, endothelial cell marker von Willebrand factor (vWF), α-SMA, and vimentin, consequently leading to enhanced endothelial-to-mesenchymal transition (EndMT) [31]. Here, VIM is linked to colorectal cancer.