Fig. 7: KAT2B activates EMT progression.

a GSEA plot showing significantly enriched pathways in siKAT2B+Dox vs siSCR+Dox MCF7ras+SS cells. p-value was calculated from gene set enrichment analysis (see details in “Methods”). b Western blot analysis of ECM1 and CD44 in MCF7ras+SS cells treated with or without GA and AA. GAPDH was used as the loading control. Images and blots are representative of three independent experiments. c qRT-PCR analysis of FN1 and ECM1 in GA- and AA-treated Dox-induced MCF7ras+SS cells (n = 3). d Flow cytometry analysis and quantification of the CD24^low/CD44^high population in vehicle control, GA-, and AA-treated MCF7ras+SS cells, as a function of Dox induction. e Flow cytometry analysis and quantification of the CD24^low/CD44^high population following KAT2B overexpression in MCF7ras+SS cells. Vector control (GFP only; pCAGIG) and KAT2B-overexpression (KAT2B+GFP; pCAGIG-KAT2B) plasmids were transfected into MCF7ras+SS cells, respectively. The GFP⁻ and GFP⁺ populations were isolated and analyzed for the CD24^low/CD44^high population (n = 3). f, g Patient-derived breast cancer organoids were transduced with scrambled shRNA or two independent KAT2B or NELF-E shRNAs, followed by western blot and sphere-formation assay (n = 3). β-actin was used as the loading control. h Patient-derived breast cancer organoids were transduced with vector control or KAT2B overexpressing plasmid, followed by western blot and sphere-formation assay (n = 4). GAPDH was used as the loading control. Blots and images are representative of at least three independent experiments. p-values in (c–h) are determined by a two-tailed Student’s t-test. Mean ± SD is represented by bar graphs. Source data are provided as a Source Data file.