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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: The emerging role of ISWI chromatin remodeling complexes in cancer

Fig. 3

Representative models of ISWI-IF/cofactor interplay. ISWI family proteins regulate cell phenotypes via association with TF/cofactor, in which the ISWI–TF/cofactor interplay is critical for optimal TF activity. A WASH recruits the NURF complex to the c-Myc promoter through VCA domain-dependent nuclear actin nucleation, which initiates c-Myc expression and maintains the self-renewal and differentiation potential of LT-HSCs [38]. B In liver CSCs. ZIC2 recruits the NURF complex to the OCT4 promoter, accompanied by enrichment of H3K4me3 and increased chromatin accessibility of OCT4, which activates OCT4 transcription and drives the self-renewal of liver CSCs [39]. C BPTF functions as a crucial cofactor of c-MYC required for tumorigenesis. The BPTF requirement for target recognition by c-MYC depends on the epigenetic context: it is dispensable for c-MYC to bind with H3K4me3-rich ‘high-affinity’ promoters and is also necessary for c-MYC to bind with ‘low-affinity’ sequences. BPTF leads to increased c-MYC recruitment to target DNA and regulates chromatin accessibility at c-MYC target promoters, thus increasing c-MYC target gene transcription and driving tumorigenesis [99,100,101]

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