DDX17 and cancer: In most instances, DDX5 phosphorylation facilitates cell proliferation and invasion; the acetylation of DDX5/DDX17 enhances their transcriptional coactivation abilities; K48 ubiquitination is responsible for DDX5 degradation; K63-polyubiquitination of DDX17 regulates miRNA biogenesis and histone modification, leading to the increase of cancer stem-like features; sumoylation elevates the stability of DDX5/DDX17 and promotes their inhibitory transcriptional activity.