fig4

Chronic activation of MUC1-C in wound repair promotes progression to cancer stem cells

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].

Journal of Cancer Metastasis and Treatment
ISSN 2454-2857 (Online) 2394-4722 (Print)

Portico

All published articles are preserved here permanently:

https://www.portico.org/publishers/oae/

Portico

All published articles are preserved here permanently:

https://www.portico.org/publishers/oae/