Journal
CLINICAL AND TRANSLATIONAL MEDICINE
Volume 13, Issue 3, Pages -Publisher
JOHN WILEY & SONS LTD
DOI: 10.1002/ctm2.1201
Keywords
cancer; CDK11; OTS964; pladienolide B; spliceosome; splicing
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Human cyclin-dependent kinases (CDKs) play a crucial role in regulating the cell cycle and transcription. Despite their involvement in basic cellular processes, CDKs are often dysregulated in tumors and are promising targets for cancer therapy. CDK11, an essential gene for the growth of many malignancies, has previously had an unclear cellular function, and the mode-of-action of the first CDK11 inhibitor, OTS964, was unknown. However, recent research has shown that OTS964 prevents spliceosome activation, revealing CDK11's key role in pre-mRNA splicing regulation. This study discusses the therapeutic potential of CDK11 in cancer treatment.
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.
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