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Discovery of New Function of Mitochondria

Discovery of New Function of Mitochondria

Mitochondria, tiny structures present in most cells, are known for their energy-generating machinery. Now, Salk researchers have discovered a new function of mitochondria: they set off molecular alarms when cells are exposed to stress or chemicals that can damage DNA, such as chemotherapy. The results, published online in Nature Metabolism on December 9, 2019, could lead to new cancer treatments that prevent tumors from becoming resistant to chemotherapy.

“Mitochondria are acting as a first line of defense in sensing DNA stress. Most of the DNA that a cell needs to function is found inside the cell’s nucleus, packaged in chromosomes and inherited from both parents. But mitochondria each contain their own small circles of DNA (called mitochondrial DNA or mtDNA), passed only from a mother to her offspring. And most cells contain hundreds — or even thousands — of mitochondria.cells respond to improperly packaged mtDNA similarly to how they would react to an invading virus — by releasing it from mitochondria and launching an immune response that beefs up the cell’s defenses.

To destroy cancer, doxyrubicin targets the nuclear DNA. But the new study found that the drug also causes the damage and release of mtDNA, which in turn activates ISGs. This subset of ISGs, the group discovered, helps protect nuclear DNA from damage — and, thus, causes increased resistance to the chemotherapy drug mitochondrial stress in melanoma cancer cells, the cells became more resistant to doxyrubicin when grown in culture dishes and even in mice, as higher levels of the ISGs were protecting the cell’s DNA.

“Perhaps the fact that mitochondrial DNA is present in so many copies in each cell, and has fewer of its own DNA repair pathways, makes it a very effective sensor of DNA stress.

The mtDNA is more prone to damage — it acts like a canary in a coal mine to protect healthy cells. But in cancer cells, it means that doxyrubicin — by damaging mtDNA first and setting off molecular alarm bells — can be less effective at damaging the nuclear DNA of cancer cells. To prevent damage to mitochondrial DNA or its release during cancer treatment might prevent this form of chemotherapy resistance.

mtDNA is damaged and released and which DNA repair pathways are activated by the ISGs in the cell’s nucleus to ward off damage. The work and the researchers involved were supported by grants from the National Institutes of Health, the Cancer Prevention and Research Institute of Texas, the Office of the Assistant Secretary of Defense for Health Affairs.

By -Asst. Professor – Ms. Kumud Misra
Department -EDUCATION
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