Fig. 6: Lipidomic analysis revealed a role of SOX2 in inhibiting very long chain fatty acid synthesis. | Nature Communications

Fig. 6: Lipidomic analysis revealed a role of SOX2 in inhibiting very long chain fatty acid synthesis.

From: SOX2 drives esophageal squamous carcinoma by reprogramming lipid metabolism and histone acetylation landscape

Fig. 6

a Volcano plot of lipidomic results showing fatty acids with significant alteration upon SOX2 knockdown in K30 cells. Group comparisons were performed using unpaired two-tailed Student’s t-tests, with false discovery rate (FDR) adjustment for multiple comparisons (Benjamini-Hochberg procedure). Significance threshold was set at q < 0.05. b, c Heatmap of dysregulated TGs (b) and carnitines (c) in SOX2 knockdown vs control K30 cells. d-f Scatter plots showing alteration of very long chain TGs in SOX2 KD K30 cells (d), SOX2 overexpressing K30 cells (e), and ACSL5 overexpressing K30 cells (f). g Oil-red staining assay comparing lipid droplets in control DMSO- treated and C646 (20 μM) treated K450 cells. h Western blot showing that C646 treatment markedly downregulated histone H3 and H4 acetylation in K30 and K450 cells. Antibodies against SOX2, ACTIN, EP300 and H3 were probed on the same gel. The samples originate from the same experiment, H3ac and H4ac were processed on separate gels in parallel. Quantifications of Oil red staining are shown in (g), 3 independent experiments. Scale bar, 20 μm. Data represented as mean ± SD; ns, P  >  0.05, *P  <  0.05, **P  <  0.01, ***P  <  0.001. Student’s t test (unpaired, two-tailed). Data in a–f are from four biological replicates, n = 4. In h experiments were repeated independently at least 2 times with similar results. Representative data is shown. Source data are provided in the Source Data file.

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