Science, Space and Technology News 2024
Researchers at Johns Hopkins Medicine have identified a molecular pathway in human breast and lung cells that might lead to excessive genome duplication, a common feature in cancer cells. By studying the cell cycle, they discovered that certain proteins and enzymes behave abnormally under stress, potentially leading to cancer. These insights could help develop new cancer therapies that target these molecular abnormalities, potentially preventing cancer progression.
“An enduring question among scientists in the cancer field is: How do cancer cell genomes get so bad?” says Sergi Regot, Ph.D., associate professor of molecular biology and genetics at the Johns Hopkins University School of Medicine. “Our study challenges the fundamental knowledge of the cell cycle and makes us reevaluate our ideas about how the cycle is regulated.
Watch this video of a cell going through the cell cycle stage of duplicating its genome twice without dividing. Bright points appear in the cell’s nucleus indicating where DNA is being replicated. Credit: Sergi Regot lab, Johns Hopkins Medicine They saw that a variety of CDKs activated at different times during the cell cycle. After the cells were exposed to an environmental stressor, such as a drug that disrupts protein production, UV radiation, or so-called osmotic stress , the researchers saw that CDK 4 and CDK 6 activity decreased.Then, five to six hours later, when the cells started preparations to divide, CDK 2 was also inhibited.
Through another series of experiments, the team linked an increase in activity of so-called stress-activated protein kinases to the small percentage of cells that skirt the quiet stage and continue to double their genome.
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