Fig. 7: The PPARγ acetylation-specific signature (PASS) has predictive value for human breast cancer outcomes.

A Derivation of the PPARγ acetylation site-specific gene expression signature was based on the intersection of the genes differentially regulated by PPARγ1 WT vs. the PPARγ1 K154/155Q in MCF10A-NeuT breast cancer cells and is shown by the Venn diagram. B PPARγ acetylation site-specific ChIP-Seq was derived by comparing the ChIP-Seq of the PPARγ1 WT and PPARγ1 K154/155Q mutant. Genes bound by PPARγ1 within 10 kb upstream of the transcription start site (TSS), 10 kb downstream of the TSS and within the gene were generated for PPARγ1 WT or PPARγ1 K154/155Q. Genes only bound by in a manner dependent upon the PPARγ acetylation site (5162) were applied for the pathway analysis. C The PPARγ acetylation site-specific signature (PASS) generation was derived by the intersection of the PPARγ acetylation site-specific gene expression and ChIP-Seq. The top 23 up-regulated genes (>2 fold) were selected for the clinical analysis. D–F Kaplan-Meier survival curves for distant metastasis-free survival (DMFS) and overall survival (OS) in subsets of breast cancer samples and F human breast cancer subtypes.