Journal article
β2-Adrenoceptors on tumor cells play a critical role in stress-enhanced metastasis in a mouse model of breast cancer
A Chang, CP Le, AK Walker, SJ Creed, CK Pon, S Albold, D Carroll, ML Halls, JR Lane, B Riedel, D Ferrari, EK Sloan
Brain Behavior and Immunity | ACADEMIC PRESS INC ELSEVIER SCIENCE | Published : 2016
Abstract
Chronic stress accelerates metastasis – the main cause of death in cancer patients – through the activation of β-adrenoceptors (βARs). We have previously shown that β2AR signaling in MDA-MB-231HM breast cancer cells, facilitates invadopodia formation and invasion in vitro. However, in the tumor microenvironment where many stromal cells also express βAR, the role of β2AR signaling in tumor cells in metastasis is unclear. Therefore, to investigate the contribution of β2AR signaling in tumor cells to metastasis in vivo, we used RNA interference to generate MDA-MB-231HM breast cancer cells that are deficient in β2AR. β2AR knockdown in tumor cells reduced the proportion of cells with a mesenchyma..
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Awarded by National Science Foundation
Funding Acknowledgements
The authors thank Dr. Kaylene Simpson from the Victorian Centre for Functional Genomics at Peter MacCallum Cancer Center for assistance with shRNA techniques, Dr. Bronwyn Evans from Monash University for the beta<INF>2</INF>AR-GFP construct, and the Imaging, Flow Cytometry and Analysis Core at Monash Institute of Pharmaceutical Sciences for imaging and data analysis support. This research was supported by the Australian National Health and Medical Research Council (1008865), the Australian Research Council (LE110100125), the National Cancer Institute (CA160890), a National Breast Cancer Foundation fellowship to Adam K. Walker (PF-15-014), a National Health and Medical Research Council RD Wright Fellowship to Michelle L. Halls (1061687), Monash Institute of Pharmaceutical Sciences-Drug Discovery Biology (MIPS-DDB) Strategic Funding, the David Skewes Foundation and the Peter MacCallum Cancer Foundation.