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. Author manuscript; available in PMC: 2022 May 9.
Published in final edited form as: J Cancer Metastasis Treat. 2022 Mar 31;8:12. doi: 10.20517/2394-4722.2022.03

Figure 4.

Figure 4.

MUC1-C couples activation of NF-κB, MYC, and E2F in inducing the repressive PRC1 and PRC2 complexes. MUC1-C forms distinct complexes with NF-κB, MYC, and E2F1. A. MUC1-C/MYC and MUC1-C/NF-κB complexes activate PRC1 by inducing BMI1, RING2, and RING1. B. The MUC1-C→E2F and MUC1-C→NF-κB pathways activate PRC2 by inducing EZH2, SUZ12, and EED. C. Schema depicting the integration of MUC1-C-induced activation of E2F and NF-κB in driving EZH2 expression (BioRender). These pathways and those shown in Figures 3 and 5 are highlighted to emphasize the capacity of MUC1-C to integrate the activation of multiple effectors that reprogram the epigenome. The formation of specific MUC1-C complexes on the promoters and enhancers of target genes has also been summarized elsewhere[23,24].