A study led by the University of Colorado Boulder provides insight on the behavior of a cell protein that could lead to new therapies for hard-to-treat cancers.

The study, published by the Genes and Development journal, looks into the protein Cyclin Dependent Kinase 7 (CDK7) that helps all cell types decode the genetic instructions provided by their DNA.

Scientists know that CDK7 can be used by cancer cells, fueling the cells to multiply out of control.

To combat this, scientists have tried to develop CDK7-inhibitors; however, early clinical trials have been disappointing because of a lack of understanding of what CDK7 does.

The study aimed to fill this informational gap.

For the first time, the research team identified the hundreds of proteins that CDK7 switches on or off, providing unprecedented insight into its influence.

The study also found that CDK7 plays a role in multiple stages of decoding, regulates other key enzymes and can be made inactive when attached to larger 10-protein complex TFIIH.

“These findings could have broad biomedical application,” said lead author Dylan Taatjes, a professor in CU’s Department of Biochemistry.

Scientists are beginning trials to administer the latest version of CDK7 inhibitors to drug-resistant breast, colorectal, lung, ovarian and pancreatic cancer patients.

Taatjes said the study findings suggest these trials hold promise.

The study was conducted in collaboration with scientists from the Syros and Paraza pharmaceutical companies, the University of Colorado School of Medicine and the BioFrontiers Institute.

The full study is available at genesdev.cshlp.org.