β-ARs signal cooperatively with mutant EGFR and inactivate LKB1

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Fig. S1 1 Oxygen consumption rate (pmol/sec/10⁶cells) shLKB1#1 control * untreated 25 μM erlotinib H358 Vector LKB1 Oxygen consumption rate (pmol/sec/10⁶cells)

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Volume 16, Issue 6, Pages (August 2016)

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Fig. 2. β-ARs signal cooperatively with mutant EGFR and inactivate LKB1. β-ARs signal cooperatively with mutant EGFR and inactivate LKB1. (A) NSCLC cells harboring wild-type EGFR or EGFR-activating mutations were stimulated with NE (10 μM), and IL-6 secretion was measured by ELISA. *P ≤ 0.001. Data are means ± SD. (B) Coimmunoprecipitation of endogenous β2-AR and EGFR in HCC827 cells (EGFR mutant) after NE stimulation. (C) HCC827 (EGFR mutant) and A549 (EGFR wild-type) cells were transfected with control vector or a FLAG-tagged β2-AR expression vector. After treatment with NE, cells were immunostained with antibodies directed against EGFR or FLAG-tag and assessed by Duolink proximity ligation assay. Data are means ± SD. (D) Representative images from Duolink assay. Red foci indicate interactions between endogenous EGFR and FLAG-tagged β2-AR. Scale bar, 10 μm. (E) Heatmap depicting mean protein expression after treatment with NE (10 μM; 15 min). (F) Alterations in phosphorylation of LKB1 at the inhibitory site S428, AMPK activation, and mechanistic target of rapamycin (mTOR) activity (p70S6K) after NE stimulation as determined by RPPA. Data are means ± SD. (G) RPPA results were confirmed by Western blotting. (H) Western blot demonstrating the effect of NE (10 μM; 15 min) on the phosphorylation of LKB1 at the inhibitory site S428 and phosphorylation of mTOR and p70S6K in H1975 cells. Monique B. Nilsson et al., Sci Transl Med 2017;9:eaao4307 Published by AAAS