New CDK strategies could target tumor growth by shutting down key gene activity
Cancer is the second-leading cause of death in Germany. In the search for new therapeutic approaches that target the uncontrolled growth of tumor cells, a class of enzymes known as cyclin-dependent kinases (CDKs) has come into focus. This family of enzymes plays a fundamental role in gene expression and cell division. An overview of the current state of research on the transcriptional regulation…
Cancer remains a leading cause of mortality in Germany. Researchers are exploring novel therapeutic strategies to target the unchecked proliferation of tumor cells. One focus has been the family of enzymes known as cyclin-dependent kinases (CDKs), which play a crucial role in gene expression and cell division.
An overview of recent research on the transcriptional regulation of CDKs and their potential in cancer treatment was compiled by researchers from University Hospital Bonn and the University of Bonn, in collaboration with Robert P. Fisher from the Icahn School of Medicine at Mount Sinai. The findings have been published in Nature Reviews Drug Discovery.
Cancer development often involves alterations in gene expression, regulated by RNA polymerase II, which transcribes DNA into messenger RNA for protein synthesis. Disruption of these regulatory mechanisms can lead to the development of malignant cells. CDKs control gene activity by influencing RNA polymerase II and transcription factors through the addition of phosphate groups. Inhibiting individual CDKs can reduce gene expression, altering the processing of messenger RNA.
Given that cancer cells frequently rely on specific genetic programs for growth and survival, new drugs can specifically target CDKs involved in pathological genetic programs, thereby targeting tumor cells more effectively while sparing healthy tissue. Currently, four active substances targeting CDK4 and CDK6 are used to treat HR+/HER2-negative breast cancer.
Clinical trials are also exploring their efficacy in prostate cancer. Geyer and Fisher provide a comprehensive overview of modern strategies for developing new CDK agents, including classic inhibitors and innovative technologies like PROTACs and molecular glues, which can degrade disease-relevant proteins or rewire cellular signaling pathways.
Combining these substances with existing therapies, such as immunotherapies or PARP inhibitors, holds promise for increasing efficacy. However, the authors highlight the challenge of ensuring that these drugs act with high precision to minimize toxicity to healthy cells.
The convergence of advances in structural biology, chemistry, and cancer research is opening new therapeutic avenues against cancer and inflammatory diseases, such as rheumatoid arthritis.
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