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        Activation of β2-Adrenergic Receptor Promotes Growth and Angiogenesis in Breast Cancer by Down-regulating PPARγ

        Jing Zhou,Zhanzhao Liu,Lingjing Zhang,Xiao Hu,Zhihua Wang,Hong Ni,Yue Wang,Jun-fang Qin 대한암학회 2020 Cancer Research and Treatment Vol.52 No.3

        Purpose Chronic stress and related hormones are key in cancer progression. Peroxisome proliferator- activated receptor ! (PPAR!) and its agonists was reported that inducing anti-tumor effect. However, the function of PPAR! in pro-tumorigenic effects induced by chronic stress in breast cancer remains unknown. Herein, we have characterized a novel role of PPAR! and vascular endothelial growth factor (VEGF)/fibroblast growth factor 2 (FGF2) signals in breast cancer promoted by chronic stress. Materials and Methods We performed experiments in vivo and in vitro and used bioinformatics data to evaluate the therapeutic potential of PPAR! in breast cancer promoted by stress. Results Chronic stress significantly inhibited the PPAR! expression and promoted breast cancer in vivo. VEGF/FGF2-mediated angiogenesis increased in the chronic stress group compared to the control group. PPAR! agonist pioglitazone (PioG) injection offset the pro-tumorigenic effect of chronic stress. Moreover, specific "2-adrenergic receptor ("2R) antagonist ICI11- 8551 inhibited the effect of chronic stress. In vitro, norepinephrine (NE) treatment had a similar tendency to chronic stress. The effect of NE was mediated by the "2R/adenylate cyclase signaling pathway and suppressed by PioG. PPAR! suppressed VEGF/FGF2 through reactive oxygen species inhibition. Bioinformatics data confirmed that there was a low PPAR! expression in breast invasive carcinoma. Lower PPAR! was associated with a significantly worse survival. Conclusion "2R activation induced by chronic stress and related hormones promotes growth and VEGF/ FGF2-mediated angiogenesis of breast cancer by down-regulating PPAR!. Our findings hint that " receptor and PPAR! as two target molecules and the novel role for their agonists or antagonists as clinical medicine in breast cancer therapy.

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