Fig. 5

ISWI-mediated EMT regulation is critical for tumor progression. ISWI proteins function as cofactors together with specific TFs to modulate EMT-related genes in a context-dependent manner. A In cervical cancer, NKX6.1 directly represses vimentin by interacting with the RBBP7 corepressor, accompanied by an increased H3K27me3 level. Meanwhile, NKX6.1 directly activates E-cadherin by interacting with the BAF155 coactivator with an increased H3K9 acetylation level [105]. B In lung cancer cells, RBBP7 acts as a transcriptional activator of the E-cadherin gene by binding to its promoter region, thereby repressing EMT progression [106]. C Normally, RBBP7, as a corepressor, interacts with HNF1B to repress SLUG transcription and EMT progression. In prostate cancer, upregulation of EZH2 suppresses the levels of the RBBP7/HNF1B transcriptional complex via direct inhibition of HNF1B expression, promoting SLUG transcription and EMT progression [107]. D RBBP7, as a corepressor, suppresses E-cadherin by interacting with TWIST and recruiting the complex to proximal regions of the E-cadherin promoter, thus inducing EMT [108]