1. Fig. 1. IL-6 is associated with resistance to EGFR TKIs and is induced by stress hormones.
IL-6 is associated with resistance to EGFR TKIs and is induced by stress hormones. (A) IL-6 secretion in NSCLC cells with acquired resistance to EGFR TKIs. Data are means ± SD. (B) Median OS in NSCLC patients with high or low circulating concentrations of IL-6 treated with erlotinib. (C) mRNA expression of ADRB1,2,3 in 159 patient samples (left) and in 116 NSCLC cell lines (right). (D) NSCLC cells were stimulated with NE (24 hours). IL-6 secretion was determined by ELISA. *P ≤ Bars are means ± SEM. (E) IL-6 mRNA expression after NE stimulation (10 μM for 3 hours). *P ≤ Data are means ± SD. (F) NE-induced IL-6 secretion after treatment with the β-AR inhibitor propranolol (PPL; 1 μM) or the α-AR inhibitor phentolamine hydrochloride (1 μM). *P ≤ 0.01; one-way analysis of variance (ANOVA). Data are means ± SD. (G) IL-6 production after treatment with a β1-AR agonist (dobutamine; 50 μM) or a β2-AR agonist (salbutamol; 50 μM) for 24 hours. *P ≤ 0.02; one-way ANOVA. Data are means ± SD. (H) Effect of the adenylyl cyclase activator forskolin (10 μM) on IL-6 secretion. *P ≤ P value calculated by two-tailed Student’s t test. (I) Circulating concentrations of IL-6 in NSCLC patients with or without incidental pan β-blocker use (BB; *P = 0.02). Data are means ± SEM.
Monique B. Nilsson et al., Sci Transl Med 2017;9:eaao4307
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