CXCL8 and cancer: Under in vitro conditions, they stimulated cancer cell proliferation (via IL-6), migration (via CXCL8/IL-8 and CCL2/MCP-1), and invasion (via IL-6, MMP-3 and uPA), and they triggered the EMT in a mechanism involving TGF-β1-dependent induction of Smad 2/3-Snail1 signaling.