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. 2019 Mar 22;13(5):981–1001. doi: 10.1002/1878-0261.12473

Figure 2.

Figure 2

Model of the epigenetic mechanisms exploited by ΔNp63 to repress transcription in various SCC. (A) In HNSCC cells, ΔNp63 may recruit the histone deacetylates HDAC1 and HDAC2 to chromatin, preventing transcription factor binding to the promoters of pro‐apoptotic genes, such as PUMA. (B) In lung SCC cells, ΔNp63 is able to repress the transcription of anti‐proliferative genes by promoting H2A.Z incorporation. (C) In HNSCC cells, ΔNp63 interacts with the SWI/SNF subunit ACTL6A, inducing the repression of anti‐proliferative genes.