Fig. 4: SREBF1 promotes biosynthesis of fatty acids, SL, and GPL in SCCs.

a qRT-PCR measuring mRNA levels of central enzymes for fatty-acid synthesis upon knockdown of SREBF1 in ESCC cells. Mean ± SEM are shown, n = 3 (biological replicates). *P < 0.05; **P < 0.01; P-values were determined by a two-sided t-test. b, c Western blotting analyses showing protein levels of central enzymes for fatty-acid synthesis upon either b knockdown of SREBF1 or c treatment with Fatostatin (0, 3.25 μM, 6.5 μM, 13 μM) in ESCC cells. The western blotting experiments were performed in three biologically independent replicates, and the representative result were shown here. d Volcano plot of LC-MS/MS-based lipidomics after treatment with Fatostatin in KYSE510 cells. Each dot is one lipid ion. e Scatter plot of significantly changed lipid ions, which were grouped by lipid classes. Each dot is one lipid ion. SL sphingolipids, GPL glycerophospholipids, GL glycerolipids. f Schematic diagram showing the regulation of lipid synthesis pathways by SREBF1 via integration of RNA-Seq (SREBF1 knockdown vs scramble) and ChIP-Seq in TE5 cells. FA fatty acid, SL sphingolipid, GPL glycerophospholipids, MUFA monounsaturated FAs, PUFA polyunsaturated FAs, 3kSN 3-keto-sphinganine, SA sphinganine, SPT serine palmitoyltransferase, DHCer dihydroceramide, CER ceramide, CerG1 glucosylceramide, CerG2 giglucosylceramide, CerG3 triglucosylceramide, SM sphingomyelin, SO Sphingosine, S1P sphingosine 1 phosphate, G3P glycerol 3-phosphate, LPA lysophosphatidic acid, PA phosphatidic acid, DAG diacylglyceride, PG phosphatidylglycerol, CL cardiolipin.