The discovery could lead to new treatments and stop cancer growth.
Scientists at Johns Hopkins School of Medicine have uncovered a molecular pathway that lures cells into the genome duplication pathway that is characteristic of cancer cells. This could lead to new treatments and halt cancer growth.
was announced on sciencethis research reveals the consequences of the molecules and enzymes that trigger and control the process of making new cells from a cell’s genetic material.
Cells follow an orderly routine that begins by making a copy of the entire genome, separating the copies of the genome, and dividing the replicated DNA equally between two “daughter” cells.
The stressed cells may then be at risk of accidentally copying their genome again.
Focusing on human cells lining breast ducts and lung tissue, scientists analyzed thousands of images of single cells as they undergo cell division, and discovered cyclins, which play a key role in cell cycle control. We developed a luminescent biosensor for tagging dependent kinases (CDKs).
The researchers found that different CDKs are activated at different times in the cell cycle and observed that the activity of CDK 4 and CDK 6 decreased after exposure to environmental stressors.
Up to 6 hours after cells begin to prepare to divide, just before mitosis, when cells pull apart and divide, a protein complex known as the anaphase promoting complex (APC) is activated, while CDK 2 inhibited.
The researchers observed that up to 10% of breast and lung cells returned to the cell cycle and their chromosomes divided again, and found that the drug combination “replicated the genomes of some cancer cells twice, resulting in This suggests that there is a possibility of creating heterogeneity in the drug resistance,” explained Serge Rego, associate professor of molecular biology and genetics at the Johns Hopkins University School of Medicine.
He added: “There may be drugs that can block APC activation before mitosis, preventing cancer cells from replicating their genome twice and preventing tumor progression. No,” he continued.
