Can Cancer Cells Be Turned Off?
A study led by scientists at the Case Comprehensive Cancer Center at Case Western Reserve University in Cleveland, Ohio, and the University of Michigan Rogel Cancer Center in Ann Arbor have identified a binding site where drug compounds could stabilize a key braking mechanism in cancer cells.
A study led by scientists at the Case Comprehensive Cancer Center at Case Western Reserve University in Cleveland, Ohio, and the University of Michigan Rogel Cancer Center in Ann Arbor have identified a binding site where drug compounds could stabilize a key braking mechanism in cancer cells — essentially stopping the growth of many types of cancer.
Past studies showed certain molecules were capable of increasing the activity of the tumor suppressor protein PP2A, but researchers lacked information about the physical site where the molecules interact with the protein. As noted in “Selective PP2A Enhancement Through Biased Heterotrimer Stabilization,” this new discovery may lead to the development of anti-cancer drugs that enhance tumor suppressing proteins. In their research, the team used cryo-electron microscopy to render three-dimensional images of the tool-molecule DT-061 (which is bound to PP2A). This allowed them to see how parts of the protein come together and are stabilized. Reporting in Cell, they explain the binding pocket is where PP2A interacts with its phosphatase target to stabilize interactions between individual PP2A subunits.
In addition to cancer cells, PP2A also dysregulated cardiovascular and neurodegenerative diseases — a development that could lead to new medicines against these and other chronic conditions.
From Decisions in Dentistry. June 2020;6(6):7
