Housing temperature-induced stress drives therapeutic resistance in murine tumour models through β2-adrenergic receptor activation

Jason W.-L. Eng, Chelsey B. Reed, Kathleen M. Kokolus, Rosemarie Pitoniak, Adam Utley, Mark J. Bucsek, Wen Wee Ma, Elizabeth A. Repasky () and Bonnie L. Hylander ()
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Jason W.-L. Eng: Roswell Park Cancer Institute, Center for Genetics and Pharmacology
Chelsey B. Reed: Roswell Park Cancer Institute, Center for Genetics and Pharmacology
Kathleen M. Kokolus: Roswell Park Cancer Institute, Center for Genetics and Pharmacology
Rosemarie Pitoniak: Roswell Park Cancer Institute, Center for Genetics and Pharmacology
Adam Utley: Roswell Park Cancer Institute, Center for Genetics and Pharmacology
Mark J. Bucsek: Roswell Park Cancer Institute, Center for Genetics and Pharmacology
Wen Wee Ma: Roswell Park Cancer Institute
Elizabeth A. Repasky: Roswell Park Cancer Institute, Center for Genetics and Pharmacology
Bonnie L. Hylander: Roswell Park Cancer Institute, Center for Genetics and Pharmacology

Nature Communications, 2015, vol. 6, issue 1, 1-13

Abstract: Abstract Cancer research relies heavily on murine models for evaluating the anti-tumour efficacy of therapies. Here we show that the sensitivity of several pancreatic tumour models to cytotoxic therapies is significantly increased when mice are housed at a thermoneutral ambient temperature of 30 °C compared with the standard temperature of 22 °C. Further, we find that baseline levels of norepinephrine as well as the levels of several anti-apoptotic molecules are elevated in tumours from mice housed at 22 °C. The sensitivity of tumours to cytotoxic therapies is also enhanced by administering a β-adrenergic receptor antagonist to mice housed at 22 °C. These data demonstrate that standard housing causes a degree of cold stress sufficient to impact the signalling pathways related to tumour-cell survival and affect the outcome of pre-clinical experiments. Furthermore, these data highlight the significant role of host physiological factors in regulating the sensitivity of tumours to therapy.

Date: 2015
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DOI: 10.1038/ncomms7426

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