A new finding about how the body's DNA repair process works may lead to new chemotherapy treatments.

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Florida State University College of Medicine researchers have discovered a new way of studying the body’s DNA repair mechanism, which might lead to novel chemotherapeutic therapies for various illnesses.

One of the most puzzling aspects of modern medicine is the ability of broken DNA to be repaired, yet the pathways involved in this repair process change as cells go through their life cycle.

It’s called base excision repair, and it’s a process in which the damaged material is removed, and DNA is created to fill in and then close the gaps.

According to the findings of F.S.U. Researchers led by Eminent Professor Zucai Suo, it is possible to boost the efficiency of BER via an inherent process that occurs only at a particular period in the cell life cycle.

Proceedings of the National Academy of Sciences is the journal in which this research is published.

Polymerase beta (PolyB) is an enzyme in BER that does two things: it produces DNA, and it starts a process to clear up the “chemical garbage” that’s left behind.

Researchers at Suo’s laboratory have discovered that by trapping PolyB when it is naturally cross-linked with DNA, the enzyme may produce new genetic material 17 times quicker than when the two are not cross-linked. It is possible that PolyB’s two roles are intertwined during BER.

Researchers are learning more about how chemotherapy affects cellular genomic stability as well as therapeutic effectiveness and resistance.

According to Suo, a lot of damage is done to DNA in cancer cells when they multiply rapidly. Damage to cancer cells’ DNA occurs when a doctor administers particular medications to combat the disease.

Cancer cells that cannot repair DNA damage on time will perish. Alternatively, the cancerous cells can evade treatment and develop resistance.

Instead of simulating the process, this study looked at PolyB and naturally related DNA. Scientists were aware of the role of BER enzymes before this discovery but were unable to comprehend how they interacted thoroughly.

No one on the study team, but Penn State University professor of biochemistry and molecular biology Thomas Spratt, noted that nicks in DNA might lead to unpleasant things like DNA double-strand breaks. In his research, Zucai discovered a previously unknown phenomenon, and he accomplished this by using a variety of ways.

The researchers created a new BER route and are now testing it in human cells, exposing PolyB’s functional dynamics.

According to the Researcher, future study is required to dig deeper into this fundamental pathway.

Reference:

Adarsh Kumar et al, Interlocking activities of DNA polymerase β in the base excision repair pathway, PANS (2022). DOI: 10.1073/pnas.2118940119

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