Fig. 3
From: Sustained SREBP-1-dependent lipogenesis as a key mediator of resistance to BRAF-targeted therapy
SREBP-1 contributes to membrane saturation and therapy resistance. a Lipidomic (phosphatidylcholine) profiles of 451lu and 451lu R cells treated with vemurafenib (5 μM) and SREBP inhibitors fatostatin and betulin (n = 3). b Lipidomics of hetero- and homozygous CRISPR-Cas9 knockouts of SREBF-1 in combination with vemurafenib treatment (n = 3). c Proliferation curves of 451lu and 451lu R cells treated with vemurafenib and fatostatin or betulin (phase contrast density measured by the Incucyte system, raw images and bar graph are shown in Supplementary Figs. 10, 11) (n = 4). d 451lu and 451lu R cells were treated with SREBP inhibitors and vemurafenib and were assayed for their ability to form colonies in soft agar, raw images and bar graph are shown in Supplementary Fig. 12 (n = 3). e Proliferation curves of 451lu R SREBP KO cells, raw images and bar graph are shown in Supplementary Figs. 13, 14 (n = 4). f SREBF-1 KO 451lu R cells were assayed for their ability to form colonies in soft agar in presence or absence of vemurafenib, raw images and bar graph are shown in Supplementary Fig. 15 (n = 3). All data are represented as mean ± s.e.m. (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001)
