Invasive phenotype in triple negative breast cancer is inhibited by blocking SIN3A–PF1 interaction through KLF9 mediated repression of ITGA6 and ITGB1

•We show that the PAH2 domain of SIN3A is a target when it is inhibited from binding to PF1 results in inhibition of invasive phenotype in TNBC.•Epigenetic repression of integrins expression and downstream pathways results from enhanced binding of KLF9 /SIN3A repressor complex to their promoters.•Genome wide transcriptomic analysis showed downregulation of multiple invasion related genes. Tumor growth and lung metastasis were markedly decreased in vivo.•Our studies highlight that PF1 might serve as a gatekeeper for trafficking SID protein binding to PAH2 of SIN3A and has functional role in presentation of different regulatory complexes.•Blocking the function of PAH2 offers a promising targeted therapy approach for inhibiting the invasive phenotype in TNBC.