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. 2025 Dec 21;9:80. doi: 10.1038/s42003-025-09346-4

Fig. 4. CD36 inhibits mitochondrial apoptosis of BC cells treated with palmitic acid.

Fig. 4

A, B Mitochondrial membrane potential was detected by JC-10 assay. In normal cells, JC-10 concentrates in the mitochondrial matrix where it forms red fluorescent aggregates. While in apoptotic and necrotic cells, JC-10 changes to the monomeric form and stains cells in green fluorescence. Indicated NC/CD36-transfected 231(A) and shNC/shCD36-infected T-47D cells (B) were treated with 800 μM PA. 200× magnification. Scale bar: 75 μm. Ratios of JC-10 fluorescence were plotted as mean ± S.D of three independent experiments. C Indicated detached BC cells were treated with vehicle (Veh) or 800 μm palmitic acid for 24 h. Caspase 9 was examined by WB to analyze mitochondrial caspase activation. D Cells were fractionated to mitochondrial and cytosol subfraction after undergoing the same treatments above. Cytochrome C (Cyto-C) protein in mitochondrial and cytosol subtraction were detected by WB assay. β-actin was loaded as a control to cytosol subfraction, Cox-IV was loaded as a control to mitochondrial subfraction. E−H Relative mRNA and protein level of several Bcl-2 family proteins in indicated detached BC cells treated with vehicle (Veh) or 800 μm palmitic acid by RT-qPCR (E, F) and WB analysis (G). H WB analysis of the expression of Bcl-2 from xenograft models tumors. Tumors formed by EGFP-Luc-/CD36-Luc-infected MDA-MB-231 cells. Bars represent the mean ± SD of three independent experiments, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, n.s. not significant.