Fig. 1: Exposure to CSE and B[α]P upregulated glucose metabolism to promote cell proliferation and EGFR TKI resistance.
From: Cigarette smoke-induced LKB1/AMPK pathway deficiency reduces EGFR TKI sensitivity in NSCLC
a–c CSE- and -B[α]P-selected H292 cells were subjected to colony formation assays followed by staining with 1% crystal violet (top) and quantitation (bottom) (a). The cell growth of H292 CSE- and B[α]P-selected cells treated with 1 μM of erlobinib and gefitinib for 3 days were measured by MTT assays (b) and FACS analysis (c), respectively. d The changes in the expression of glycolytic-related genes by CSE exposure (GSE10718 (top) or in smokers (GSE31210 (bottom)) were analyzed in GSEA. e–g CSE- and B[α]P-selected H292 cells was analyzed the glycolytic flux (e) and 2-NBDG uptake (f). The inhibitory effects of erlotinib treatment for 4 h on the glycolytic flux in CSE- and B[α]P-selected H292 cells were measured in Seahorse Analyzer (g). h, i The parental and CSE-selected H292 cells were injected into SCID mice followed by 18FDG uptake of tumor by microPET/CT analysis (h), and the inhibitory effect of erlotinib treatment (50 mg/kg) for 3 day on the maximum SUV in tumor (T) was measured and normalized to that in muscle (M) (i). j, k The ATP level (j) and cell viability (k) of CSE- and -B[α]P-selected H292 cells were treated with 1 μM of erlotinib and gefitinib under the conditions with different glucose concentrations for 3 days. l The cell viability of CSE- and B[α]P-selected H292 cells treated with 1 μM of erlotinib/gefitinib in the presence or absence of 5 mM 2DG were measured under 1 mM glucose culture condition for 2 day. Data are shown as mean ± SEM from experiments performed in triplicate. *p < 0.05; **p < 0.01; ***p < 0.001.
