Fig. 5: Mogat1 inhibition reprograms breast cancer cell metabolism by suppressing TCA cycle activity.
From: Mogat1 drives metabolic adaptations to evade immune surveillance
a Orthogonal partial least squares discriminant analysis (OPLS-DA) score plot comparing the metabolic profiles of shCTRL and shMogat1 4T1 tumor cells (n = 3 biological replicates per group). b Volcano plot depicting differentially abundant metabolites between shCTRL and shMogat1 4T1 tumor cells. Metabolites with a variable importance in projection (VIP) score > 1 from the OPLS-DA analysis and a P < 0.05 from two-tailed unpaired Student’s t-test are highlighted. c Heatmap illustrating the relative abundance of differentially expressed metabolites (VIP > 1, P < 0.05) identified by non-targeted mass spectrometry. d Schematic diagram depicting metabolic flux from glucose and glutamine into the tricarboxylic acid (TCA) cycle and glycolysis pathways. e–g Targeted mass spectrometry analysis of TCA cycle metabolites in shCTRL and shMogat1 tumor cells. f 4T1 cells. g MMTV-PyMT cells. h B16/F10 cells. (n = 4 biological cell cultures per group). h Heatmap displaying the enrichment of KEGG metabolic pathways in shCTRL and shMogat1 4T1 tumor cells, based on gene expression data. Data are representative of two independent experiments. Data in (e, f, g) are presented as the mean ± SD. Statistical significance was determined using a two-tailed unpaired Student’s t-test. Source data are provided as a Source Data file.
