Summarizing each variant individually and assigning putative mechanism of action to specific biological processes, overexpression of AP-2α (K/A) induced a decrease in tumor cell viability (via suppression of ERK and CCND1 in Ras-Raf-MEK-ERK and Wnt pathways, or via CD133 downregulation), migratory potential (through VEGF/PEDF, β-catenin/TCF/LEF and Bax/Cytochrome c/Apaf1/Caspase 9 pathways), MMP-2 activity (hence invasive potential, through direct MMP2 suppression) and the ability of a single cell to grow into a colony (via p21WAF1/CIP1 activation). Here, CCND1 is linked to neoplasm.