Fig. 4

Gene inhibition of CAV2 altered lipid profiles and induced polyunsaturated fatty acids (PUFAs) accumulation in OSCC. (A) Heatmap for the differential expression lipids in SCC25 KD versus NC cells (n = 6 per group). (B) Statistical chart of lipid sub-classes and the corresponding number of lipid molecules in SCC25 KD and SCC25 NC cells (mean ± SD, n = 6). (C) Summary diagram of lipid changes. Levels of representative individual lipid species in SCC25 KD and NC cells. (D) Bubble chart of metabolic pathway enrichment. (E) Levels of differential PUFAs in SCC25 KD and NC cells. (F) Related heatmaps of differentially expressed FAs and other differentially expressed lipids. Significance was determined by the Student’s t-test (B and E). Correlation analysis was performed using Pearson correlation analysis (F). *P<0.05, **P<0.01, ***P<0.001. CAV2: Caveolin2; OSCC: oral squamous cell carcinoma; PUFAs, polyunsaturated fatty acids; KD: shRNA targeting CAV2, labeled with GFP for green fluorescence tracking; NC: scrambled control shRNA, labeled with GFP for green fluorescence tracking; GL, glycerolipids; GP, glycerophospholipids; SP, sphingolipids; SL, saccharolipids; OAHFA, (O-acyl)-1-hydroxy fatty acid; FA, fatty acid; DG, diglyceride; PC, phosphatidylcholine; PE, phosphatidylethanolamine; dMePE, dimethylphosphatidylethanolamine; PEt, phosphatidylethanol; PS, phosphatidylserine; PI, phosphatidylinositol; PG, phosphatidylglycerol; PA, phosphatidic acid; LPC, lysophosphatidylcholine; SM, sphingomyelin; MGDG, monogalactosyldiacylglycerol