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 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.

 

Comments:

The discovery of the therapeutic potential of cyclin-dependent kinase 11 (CDK11) in cancer has shed light on its crucial role in the regulation of pre-mRNA splicing. CDKs are a group of proteins that play a vital role in controlling the progression of the cell cycle and transcription. When CDKs become deregulated in tumors, they can contribute to uncontrolled cell growth and division, making them attractive targets for cancer therapy.

CDK11 has been identified as an essential gene for the growth of many malignancies, indicating its potential as a target for cancer treatment. However, until recently, the primary cellular function of CDK11 remained unclear, and the mode-of-action of OTS964, the first CDK11 inhibitor and antiproliferative compound, was unknown.

A recent study has provided valuable insights into the role of CDK11 and the mechanism of action of OTS964. The study demonstrated that OTS964 effectively prevents spliceosome activation, which is essential for proper pre-mRNA splicing. This finding reveals that CDK11 plays a key role in the regulation of pre-mRNA splicing, a crucial process for gene expression and cellular function.

The dysregulation of pre-mRNA splicing has been implicated in various diseases, including cancer. By inhibiting CDK11 and consequently suppressing spliceosome activation, OTS964 has shown potential as a therapeutic agent for cancer treatment. Targeting CDK11-mediated pre-mRNA splicing may disrupt the expression of specific genes involved in cancer growth and progression, providing a novel strategy to combat malignancies.

Further research is needed to fully understand the precise mechanisms by which CDK11 influences pre-mRNA splicing and its implications for cancer therapy. However, these recent findings highlight CDK11 as a promising target and provide a basis for the development of more effective therapies that specifically modulate pre-mRNA splicing in cancer cells.

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