Therapeutic potential of CDK11 in cancer

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 growt...

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Detalles Bibliográficos
Autor principal: Blazek, Dalibor
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2023
Materias:
Commentary
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9975460/
https://www.ncbi.nlm.nih.gov/pubmed/36855776
http://dx.doi.org/10.1002/ctm2.1201
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author Blazek, Dalibor
author_facet Blazek, Dalibor
author_sort Blazek, Dalibor
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description 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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spelling pubmed-99754602023-03-02 Therapeutic potential of CDK11 in cancer Blazek, Dalibor Clin Transl Med Commentary 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. John Wiley and Sons Inc. 2023-02-28 /pmc/articles/PMC9975460/ /pubmed/36855776 http://dx.doi.org/10.1002/ctm2.1201 Text en © 2023 The Authors. Clinical and Translational Medicine published by John Wiley & Sons Australia, Ltd on behalf of Shanghai Institute of Clinical Bioinformatics. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Commentary
Blazek, Dalibor
Therapeutic potential of CDK11 in cancer
title Therapeutic potential of CDK11 in cancer
title_full Therapeutic potential of CDK11 in cancer
title_fullStr Therapeutic potential of CDK11 in cancer
title_full_unstemmed Therapeutic potential of CDK11 in cancer
title_short Therapeutic potential of CDK11 in cancer
title_sort therapeutic potential of cdk11 in cancer
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9975460/
https://www.ncbi.nlm.nih.gov/pubmed/36855776
http://dx.doi.org/10.1002/ctm2.1201
work_keys_str_mv AT blazekdalibor therapeuticpotentialofcdk11incancer

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