Therapeutic potential of CDK11 in cancer
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't, Comment
Grant support
21-19266S
the Czech Science Foundation
23-04754X
the Czech Science Foundation
PubMed
36855776
PubMed Central
PMC9975460
DOI
10.1002/ctm2.1201
Knihovny.cz E-resources
- 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
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.
See more in PubMed
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