Scientists find the new way of tobacco smoke inducing cancer

A recent study by researchers at the University of Kentucky revealed a new way of tobacco smoke inducing lung cancer: inhibiting the DNA repair process, which is called nucleotide excision repair (NER). The results were published in the journal PLoS ONE. Many constituents of tobacco smoke are carcinogens that can damage DNA. This damage must be prevented by the DNA repair process to further eliminate the genetic mutation process. In this way, researchers found through recombinant human proteins that DNA repair processes such as nucleotide excision repair are critical to block the accumulation of the final DNA mutation, which drives the development of lung cancer.

"It has been determined that carcinogens in tobacco smoke can cause mutations," says Isabel Mellon, an associate professor and principal investigator in the Department of Toxicology and Cancer Biology, but only a handful of researchers have investigated the effects of tobacco smoke on DNA repair pathways influences.

Mellon and her team studied the effects of cigarette smoke concentrates (CSC), a commonly used alternative to tobacco smoke, on the nucleotide excision repair process in cultured human lung cells. They found that the addition of CSC to these cells significantly reduced nucleotide excision repair efficiency. In addition, the researchers showed that the addition of CSC stimulated the destructive nature of a key nucleotide excision repair protein called XPC. The abundance of XPC reduction can then explain how the CSC inhibits the nucleotide excision repair process.

The results indicate that tobacco smoke has a dual effect on DNA integrity: it not only impairs DNA but also inhibits the critical process of repairing DNA damage. "Inhibition of nucleotide excision repair may increase the risk of mutation and cancer, particularly in the case of chronic DNA damage induction, such as in smokers' lung problems," Mellon explained.

If this is the case, the ability of repair damaged DNA in lung cells of a given human can be used to predict the risk of lung cancer in that person due to tobacco smoke. "In the future, we want to determine how different the efficiency of the nucleotide excision repair pathway varies among people," Mellon said. "We are also continuing to study how the efficiency of human DNA repair is adversely affected by environmental factors. Whether due to genetic factors or environmental factors, reduce of DNA repair will increase the risk of cancer patients." Flarebio offers recombinant proteins of good quality such as recombinant Cdh10 at competitive prices.