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. 2020 Jul 8;20(3):2595–2605. doi: 10.3892/ol.2020.11833

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Copyright: © Fu et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 2. — Schematic of intestinal epithelium cell differentiation and the genetic interactions of genes involved in CRC progression. (A) Diagram representing ATOH1 expression and regulation during the differentiation of multiple cell lineages of the intestinal epithelium. ATOH1 is necessary for the differentiation of secretory lineages in the intestine, including enteroendocrine, goblet and Paneth cells. The differentiation of different intestinal cell types is regulated by a contrary interplay between ATOH1 and Notch signaling pathways. (B) Schematic of the CRC associated gene interaction network of ATOH1. In intestinal development, ATOH1 is required for regulating target genes, which either enhances differentiation or inhibits proliferation. However, ATOH1 is downregulated by CpG methylation or GSK3β inhibition in CRC. CRC, colorectal cancer; ATOH1, atonal bHLH transcription factor 1; GSK3β, Glycogen synthase kinase 3 β; Hes1, hes family bHLH transcription factor 1; GSK3I, GSK3 inhibitor; APC, adenomatous polyposis coli; NICD, intracellular domain of the notch protein; GSI, γ-secretase inhibitor; p27, H3 histone pseudogene 23; CSC, cancer stem cells; Ccnd1; cyclin D1; APN, adiponectin; TNF-α, tumor necrosis factor-α; SPDEF, SAM pointed domain containing ETS transcription factor; MUC2, mucin 2.