Alterations of tumor microenvironment by carbon monoxide impedes lung cancer growth

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Alterations of tumor microenvironment by carbon monoxide impedes lung cancer growth

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Title: Alterations of tumor microenvironment by carbon monoxide impedes lung cancer growth
Author: Nemeth, Zsuzsanna; Csizmadia, Eva; Vikstrom, Lisa; Li, Mailin; Bisht, Kavita; Feizi, Alborz; Otterbein, Sherrie; Zuckerbraun, Brian; Costa, Daniel B.; Pandolfi, Pier Paolo; Fillinger, Janos; Döme, Balazs; Otterbein, Leo E.; Wegiel, Barbara

Note: Order does not necessarily reflect citation order of authors.

Citation: Nemeth, Z., E. Csizmadia, L. Vikstrom, M. Li, K. Bisht, A. Feizi, S. Otterbein, et al. 2016. “Alterations of tumor microenvironment by carbon monoxide impedes lung cancer growth.” Oncotarget 7 (17): 23919-23932. doi:10.18632/oncotarget.8081. http://dx.doi.org/10.18632/oncotarget.8081.
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Abstract: We hypothesized that tumor-associated macrophages (TAMs) are controlled by the diffusible gas carbon monoxide (CO). We demonstrate that induction of apoptosis in lung tumors treated with low doses of CO is associated with increased CD86 expression and activation of mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinases (Erk) 1/2 pathway in tumor microenvironment. Presence of CD86-positive cells was required for the anti-tumoral effects of CO in established A549 xenografts. We show that the effects of CO on tumor stroma and reprogramming of macrophages towards the anti-tumoral phenotype is mediated by reactive oxygen species (ROS)-dependent activation of MAPK/Erk1/2-c-myc pathway as well as Notch 1-dependent negative feedback on the metabolic enzyme heme oxygenase-1 (HO-1). We find a similar negative correlation between HO-1 and active MAPK-Erk1/2 levels in human lung cancer specimens. In summary, we describe novel non-cell autonomous mechanisms by which the diffusible gas CO dictates changes in the tumor microenvironment through the modulation of macrophages.
Published Version: doi:10.18632/oncotarget.8081
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5029674/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:29407642
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