12 December 2012

Cancer cells age due to lack of dNTP

A new mechanism of regulation of aging of cancer cells has been discovered

Copper newsAmerican scientists have discovered a new mechanism for regulating the aging of cancer cells, reports EurekAlert! (Previously unknown mechanism identified in oncogene-induced senescence).

The results of the work of researchers from the Roswell Park Cancer Institute, conducted under the leadership of Mikhail Nikiforov, will be published in the January issue of The American Journal of Pathology.

The aging of cancer cells is considered by oncologists as one of the ways to suppress the growth of malignant neoplasms. With aging, cells lose their ability to divide, and the process of programmed cell death – apoptosis - is started in them.

Previously, it was believed that the aging of tumor cells causes excessive DNA replication, as well as damage to the cell as a result of oxidation (oxidative stress). During the study, Nikiforov and his colleagues found that the aging process of cancer cells is associated with a decrease in deoxyribonucleoside triphosphate (dNTP) reserves, which causes DNA damage. In turn, a decrease in dNTP reserves is associated with a decrease in the number of enzymes involved in its biosynthesis.

In addition, the researchers found that even partial recovery of dNTP reserves is sufficient to significantly restore DNA and suppress cell aging.

"Oncogene-induced cell aging is an important defense mechanism that suppresses the proliferation of tumor cell precursors. Our results prove that in order to damage DNA and trigger the process of cellular aging, both depletion of the dNTP reserve and excessive DNA replication are necessary," the lead author of the study emphasized.

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