Supplementary Figure 1 Legend from Synergistic Effects of Metformin Treatment in Combination with Gefitinib, a Selective EGFR Tyrosine Kinase Inhibitor, in LKB1 Wild-type NSCLC Cell Lines

Supplementary Figure 1 Legend - PDF file 52K, Effects on CALU-3, CALU-3 GEF-R, H1299, H1975 and GLC82 cell growth of the combination of metformin and gefitinib. Cell viability was determined using a 3-(4,5 methylthiazol-2-yl)-2,5- diphenyltetrazolium bromide assay. Treatment combinations and sequences are described in Materials and Methods. CI values were calculated according to the Chou and Talalay mathematical model for drug interactions using the Calcusyn software for different fractions affected (fa). CI is a quantitative measure of the degree of interaction between different drugs. If CI = 1, it denotes additivity; if CI > 1, it denotes antagonism; if 1 0.7, it denotes slight synergism; if CI = 0.7-0.3, it denotes synergism; if CI < 0.3, it denotes strong synergism. Results are the median of three independent experiments, each done in eight replicate wells for experimental point</p

Supplementary Figure 2 Legend from Synergistic Effects of Metformin Treatment in Combination with Gefitinib, a Selective EGFR Tyrosine Kinase Inhibitor, in LKB1 Wild-type NSCLC Cell Lines

Supplementary Figure 2 Legend - PDF file 58K, Supplementary Figure 2 legend: Effects on the downstream pathways by metformin treatment in A549 and H460. Western blotting analysis of AMPK, ACC, MAPK, AKT, p70S6K, S6, 4EBP1, activation following treatment with the indicated concentration of metformin. beta-actin was included as a loading control</p

Supplementary Figure 2 from Synergistic Effects of Metformin Treatment in Combination with Gefitinib, a Selective EGFR Tyrosine Kinase Inhibitor, in LKB1 Wild-type NSCLC Cell Lines

Supplementary Figure 2 - PDF file 194K, Supplementary Figure 2. Effects on the downstream pathways by metformin treatment in A549 and H460</p

Additional file 1 of ATM inhibition blocks glucose metabolism and amplifies the sensitivity of resistant lung cancer cell lines to oncogene driver inhibitors

Additional file 1: Figure S1. Expression levels of Glucose-6-phosphate dehydrogenase in H1993 and H1975 cells exposed to 100 nM KU55933 for 48 hours. Actin serves as equal loading control

Supplementary Figure 1 from Synergistic Effects of Metformin Treatment in Combination with Gefitinib, a Selective EGFR Tyrosine Kinase Inhibitor, in LKB1 Wild-type NSCLC Cell Lines

Supplementary Figure 1 - PDF file 81K, Effects on CALU-3, CALU-3 GEF-R, H1299, H1975 and GLC82 cell growth of the combination of metformin and gefitinib</p

Supplemental Figure 1 from SMO Gene Amplification and Activation of the Hedgehog Pathway as Novel Mechanisms of Resistance to Anti-Epidermal Growth Factor Receptor Drugs in Human Lung Cancer

Western blot analysis of protein levels and phosphorylated forms of MET, EGFR, MAPK, AKT, GLI1 and beta actin in protein lysates from tumors harvested from nude mice treated with the indicated drugs.</p

Supplemental Figure 2 from SMO Gene Amplification and Activation of the Hedgehog Pathway as Novel Mechanisms of Resistance to Anti-Epidermal Growth Factor Receptor Drugs in Human Lung Cancer

A) GLI1 promoter activity in EGFR-WT NSCLC cell lines. Effects of Hh and EGFR inhibition in EGFR-WT NSCLC cell lines on their abilities to B) growth, C) invade , D)migrate and E) colony forming. F)In vivo efficacy of erlotinib and LDE225 on EGFR-WT NSCLC xenografts in nude mice.</p

Supplemental Figure 3 from SMO Gene Amplification and Activation of the Hedgehog Pathway as Novel Mechanisms of Resistance to Anti-Epidermal Growth Factor Receptor Drugs in Human Lung Cancer

Graphycal representation of the interplay between Hedgehog and MET pathway.</p

Supplemental Table 1 from SMO Gene Amplification and Activation of the Hedgehog Pathway as Novel Mechanisms of Resistance to Anti-Epidermal Growth Factor Receptor Drugs in Human Lung Cancer

EGFR mutational status, gefitinib sensitivity and HH pathway activation in our panel of NSCLC cell lines.</p

Supplemental Materials and Methods from SMO Gene Amplification and Activation of the Hedgehog Pathway as Novel Mechanisms of Resistance to Anti-Epidermal Growth Factor Receptor Drugs in Human Lung Cancer

Supplemental matherial and methods</p