Human cyclin-dependent kinases (CDKs) direct the progression of the cell cycle and transcription. They are deregulated in tumours, and despite their involvement in the regulation of basic cellular processes, many CDKs are promising targets for cancer therapy. CDK11 is an essential gene for the growth of many malignancies; however, its primary cellular function has been obscure, and the mode-of-action of OTS964, the first CDK11 inhibitor and antiproliferative compound, has been unknown. A recent study has shown that OTS964 prevents spliceosome activation, revealing a key role of CDK11 in the regulation of pre-mRNA splicing. In light of these findings, we discuss the therapeutic potential of CDK11 in cancer.

• Keywords
• CDK11, OTS964, SF3B1, cancer, pladienolide B, spliceosome, splicing,
• MeSH
• Cell Division MeSH
• Cell Cycle MeSH
• Cyclin-Dependent Kinases * genetics   MeSH
• Humans MeSH
• Neoplasms * drug therapy   genetics   MeSH
• RNA Splicing MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Comment MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• CDK19 protein, human MeSH Browser
• Cyclin-Dependent Kinases * MeSH