Targeting Cyclins to Cause Cancer Cell Apoptosis

摘要: Progression through each phase of the cell cycle is precisely controlled by activity distinct cyclin-dependent kinases (CDKs) and their regulatory subunits known as cyclins. Each characterized specific cyclin-CDK combinations it tightly complex mechanisms that either allow or restrain its progression. Of these, cyclins play key role in controlling progression, with D-type being sensors for environmental cues assembly into CDK4/6 complexes leading to sequestration CDK inhibitors ultimately Cyclin E/CDK2 activation. E unique critical G1/S transition, initiation DNA replication, centrosome duplication, functions may provide underpinnings tumor development. Some functions, such oncogenic function ability, following caspase-mediated conversion a truncated form, regulate apoptosis repair, seem be independent nuclear localization associated CDK2-kinase activity. Many control genes, when deregulated, can cause cells are not dividing enter begin proliferate cancer S-phase sensitization, modulating levels E, A, CDK2 kinase useful therapeutic approach. There at present much optimism about possibility finding anticancer drug treatment strategies modulate partners. This review summarizes what biological cyclins, deregulation cancer, opportunities they targets improve clinical therapy.