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Many cancers have adapted to cope with high levels of immune system-produced free radicals, also referred to as reactive oxygen species, by overproducing antioxidant proteins. One of these proteins, superoxide dismutase 1 (SOD1), is overproduced in lung adenocarcinomas and has been implicated as a target for chemotherapy.
In this issue of the Journal of Clinical Investigation, Navdeep Chandel and colleagues from Northwestern University report the effects of a SOD1 pharmacological inhibitor on non-small-cell lung cancer (NSCLC) cells. The inhibitor, called ATN-224, stunted the growth of human NSCLC cells in culture and induced their death. The researchers also found that ATN-224 inhibited other antioxidant proteins, which caused high levels of hydrogen peroxide inside the cells. The ability of cancer cells to produce hydrogen peroxide was required for ATN-224-dependent effects, because hydrogen peroxide activated cell death pathways.
Furthermore, ATN-224 induced cancer cell death and reduced tumor sizes in a mouse model of lung adenocarcinoma. ATN-224 dependent effects in animals were improved when the inhibitor was used in combination with another drug that activates programmed cell death.
This study suggests inhibition of antioxidants may be a viable chemotherapeutic option.
Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Journal of Clinical Investigation. "Inhibition of antioxidants may be a viable chemotherapeutic option for lung cancer." Medical News Today. MediLexicon, Intl., 3 Dec. 2013. Web.
20 Apr. 2014. <http://www.medicalnewstoday.com/releases/269585>
Journal of Clinical Investigation. (2013, December 3). "Inhibition of antioxidants may be a viable chemotherapeutic option for lung cancer." Medical News Today. Retrieved from
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