Dose dependent growth inhibition of lung cancer cell-lines by erlotinib and crizotinib.

<p>(a) Exposure to erlotinib in MTS assay: HCC827 (EGFR exon 19 deletion) exhibited significant growth inhibition while A549 and H460 (wild EGFR) or H1975 (EGFR T790M resistance second mutation) were not sensitive to elrotinib. (b) Exposure to crizotinib in MTS assay: H3122 (<i>EML4-ALK</i> fusion) exhibited significant growth inhibition, while other cancer cells without a fusion gene were not sensitive to crizotinib. (c) Expression of EGFR protein and inhibition of phosphorylation by erlotinib in NSCLC cell lines in western blot analysis: Erlotinib inhibited phosphorylation of EGFR (pEGFR) in HCC827, but did not inhibit it in H1975. (d) Expression of ALK and inhibition of phosphorylation by crizotinib in NSCLC cell lines in western blot analysis: H3122 expressed ALK and crizotinib inhibited phosphorylation of ALK(pALK). (e) Exposure to erlotinib in CD-DST. (f) Exposure to crizotinib in CD-DST. Compared with MTS assay, CD-DST required lower doses of erlotinib to exhibit significant difference in growth between cell lines. <i>EGFR</i>, epidermal growth factor receptor gene; <i>EML4-ALK</i>, echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase gene.