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PUBLIC RELEASE DATE:
2-Dec-2013

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Contact: Corinne Williams
press_releases@the-jci.org
Journal of Clinical Investigation

Blocking antioxidants in cancer cells reduces tumor growth in mice

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.

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TITLE: Targeting SOD1 reduces experimental non–small-cell lung cancer

AUTHOR CONTACT: Navdeep Chandel
Northwestern University, Chicago, IL, USA
Phone: 312-503-2549; Fax: 312-503-0411; E-mail: nav@northwestern.edu

View this article at: http://www.jci.org/articles/view/71714?key=0c483873fa3d4323f67e



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