Fig. 7: CD36 upregulates BCL2 expression via the direct transcriptional regulation of YAP-TEADs.

A, B Effects of CD36 on increasing Bcl-2 were blocked after knockdown of YAP and treatment of Verteporfin or recovered after overexpression of YAP1. C, D Effects of CD36 on increasing BCL2 transcription were blocked after knockdown of YAP and treatment of verteporfin or recovered after overexpression of YAP1. E The sequence logo shows the predicted matrix profiles of the highest score. F Luciferase reporter assays of BCL2 promoter transcriptional activity. MCF-7 cells were transfected with YAP1-overexpressing plasmid or empty vector plasmid, BCL2 promoter-luciferase reporter plasmid, and Renilla luciferase plasmid for 48 h, followed by fluorescence detection. Renilla luciferase served as the transfection control. Verteporfin (10 μM) was designed to confirm the effect of YAP-TEADs-binding. G Luciferase reporter assays of mutant YAP-P3 promoter transcriptional activity. MCF-7 cells were infected with YAP1-overexpressing plasmid or empty vector plasmid, wild-type BCL2-PS promoter-reporter, and mutant reporter for 48 h, followed by fluorescence detection. (H) Chip assays were performed to verify BCL2 binding to the BCL2-PS promoter. Lane 1: BCL2 ChIP primer generated PCR product derived from 2% input DNA; Lane 2: BCL2 ChIP primer generated PCR product derived from immunoprecipitated by normal IgG; Lane 3: BCL2 ChIP primer generated PCR product derived from immunoprecipitation by an anti-YAP antibody; Lane 4: CTGF ChIP primer generated PCR product derived from immunoprecipitation by an anti-YAP antibody (I) Statistical analysis of Chip assays. Bars represent the mean ± SD of three independent experiments; *p < 0.05, **p < 0.01, ***p < 0.001.***p < 0.001.