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Death-associated protein kinase 3 (DAPK3) is a serine/threonine kinase implicated in the regulation of apoptosis, autophagy, translation, transcription, actin cytoskeleton reorganization, and smooth muscle contraction. It can induce apoptosis and autophagy, regulate myosin phosphorylation, modulate actin cytoskeleton and focal adhesion dynamics, and contribute to cell cycle progression and proliferation. DAPK3 is considered a tumor suppressor but also promotes migration and invasion in certain cancer contexts, such as triple-negative breast cancer and non-small cell lung carcinoma. Its dysregulation is implicated in cancer progression, particularly through effects on epithelial-mesenchymal transition (EMT), as well as in inflammation-associated diseases such as ulcerative colitis with risk of progression to dysplasia. No approved drugs specifically target DAPK3, but it is increasingly considered a therapeutic target in oncology and potentially in inflammatory or fibrotic diseases[1][2][5][6][8].
Inhibition of DAPK3 kinase activity reduces cell migration, invasion, and proliferation (research context); potential mechanisms include interfering with apoptosis, cell cycle, EMT, cytoskeleton organization, or autophagy[2][5][1].
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