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Schematic diagram illustrating the proposed mechanisms of the effects of KMT2B on CC. In CC cells, KMT2B promotes the expression of EGF by maintaining the status of H3K4 tri-methylation at its promoter region. CC cell-derived EGF activates EGFR and promotes the angiogenesis of endothelial cells in a paracrine manner. Meanwhile, increased EGF expression enhances the migration and invasion of CC cells in an autocrine manner by activating EGFR/PI3K/AKT pathway.
