Fig. 3: SNHG3 c.1746 A > I editing promotes fatty acid oxidation and confers ferroptosis resistance. | Communications Biology

Fig. 3: SNHG3 c.1746 A > I editing promotes fatty acid oxidation and confers ferroptosis resistance.

From: A-to-I edited SNHG3 promotes non-small cell lung cancer metastasis by promoting fatty acid oxidation and resisting ferroptosis

Fig. 3

a Correlation analysis between c.1746 A > I editing levels and gene expression in TCGA NSCLC samples (Spearman’s correlation, |r | >0.1, P < 0.05). b KEGG pathway enrichment of c.1746 A > I-associated genes. c Correlation network of c.1746 A > I with 22 genes enriched in ECM-receptor interaction, ferroptosis, and fatty acid metabolism (dot size: significance; color: correlation direction). d Quantification of mRNA expression of 22 candidate genes in SNHG3ED vs SNHG3WT cells (n = 3-5, unpaired t-test). e Western blot validation of selected targets (n = 4, unpaired t-test). f Oil Red O staining showing lipid droplet accumulation (n = 10, unpaired t-test; scale bar = 100μm). Metabolite quantification of triglycerides (g), total FFAs (h), and specific medium/long-chain FFAs (i) (n = 6, unpaired t-test). j FAO activity assessed by FAOBlue fluorescence (scale bar = 20μm). Seahorse analysis of OCR (k) and respiratory capacity (l) with Eto (CPT1 inhibitor establishing baseline FAO capacity), Oligo (ATP synthase inhibitor measuring proton leak), FCCP (Uncoupler assessing maximal respiratory capacity), and Rot/AA (Complex I/III inhibitors determining non-mitochondrial respiration) treatment (n = 5–6, one-way ANOVA with Tukey’s multiple comparisons test). m Ferroptosis sensitivity to 10 μM erastin (a ferroptosis inducer) with/without 1 μM ferrostatin-1 (a specific ferroptosis inhibitor) (n = 5, unpaired t-test). Data are mean ± SD. Significance: *P < 0.05, **P < 0.01, ***P < 0.001; ns = not significant. N indicates biological replicates.

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