Fig. 6
From: EGFR modulates monounsaturated fatty acid synthesis through phosphorylation of SCD1 in lung cancer
EGFR-stimulated lung cancer growth is dependent on SCD1 activity. a A549 stable cell lines were serum-starved overnight and then stimulated with/without EGF (10 ng/ml) for 3 days. The rates of cell proliferation were determined by CCK-8 assay in vitro. Data are mean ± SD (n = 5). b A549 cells were serum-starved overnight and then incubated with/without EGF (10 ng/ml) in the presence of 0.1% DMSO, SCD1 inhibitor-1 (MF-438) (C19H18F3N5OS) (0.1 μM) or inhibitor-2 (C20H22ClN3O3) (1 μM) for 3 days. The rates of cell proliferation were tested by CCK-8 assay in vitro. Data are mean ± SD (n = 5). c-f A549 stable cell lines ectopically expressing vector or EGFR were cultured in the medium containing 1% FBS, thus minimizing the influence of exogenously obtained MUFA from high concentrated FBS. c The transfectants were treated with 0.1% DMSO, SCD1 inhibitor-1 (0.1 μM) or inhibitor-2 (1 μM) for 2 days. The rates of cell proliferation were examined by CCK-8 assay in vitro. Data are mean ± SD (n = 5). d The transfectants were incubated with 0.1% DMSO or SCD1 inhibitor-2 (1 μM) for 24 h and cell cycle was assessed by PI staining. The percentage of cells in G1 phase or S/G2/M phase is shown. e The transfectants were treated as described in (d) and cell apoptosis was detected by Annexin V/PI staining assay. f In vitro growth was determined by colony formation assay. The representative pictures of developed colonies are shown and the number was counted after 11 days. Data are mean ± SD (n = 3). ***p < 0.001; **p < 0.01; *p < 0.05; NS, nonsignificance (when compared with the DMSO group, a-c)