Table 1.

Genes showed imprinting alteration in IBD and CRC-based studies

Gene	Location	Study	Function	Result	Refernces
NOD2 (CARD15) (IBD1)	Chr 16	Nod2−/− mice	Activates NF-kB, Controls inflammatory and immune responses	The long-lasting effects of neonatal antibiotic exposure on the microbiota and mucosal immunity may be the reason why NOD2 increases the risk of intestinal inflammation	[39]
ATG16L1	Chr 2	Transcriptomic study of UC mice model, colitis models, flora mice	Regulated the expression of lysozyme, changes the gut microbiota, inhibit necroptosis in the intestinal epithelium, increase the local Th1/Th17 response	Play role in dysbiosis and immune infiltration before disease symptoms	[40–43]
IRGM	Chr 5	Linkage analysis	Interact with autophagy, inflammation, and tumorigenesis	IRGM expression increase before the effect of bacterial autophagy, linked to UC susceptibility	[44]
IGF2	Chr 11	DNA from peripheral blood leucocytes and RNA from tumors of Chinese patients	The main role of IGF-2 is defined as a growth hormone in gestation	IGF-II LOI is present in high prevalence of CRC patients, especially, proximal cancer in Chinese population	[45]
LIT1 (KCNQ1OT1)	Chr 11	Colorectal cancer cell lines	Play role in transcriptional silencing of the KCNQ1	Play essential role in colorectal carcinogenesis	[46]
PHLDA2	Chr 11	Knockout model	Cellular apoptosis, autophagy	Downregulation of PHLDA2 inhibits tumor growth in colorectal cancer	[47]

NOD2: Nucleotide-binding oligomerization domain-containing protein 2, CARD15: Caspase recruitment domain-containing protein 15, NF-kB: Nuclear factor-kappa-B protein complex, IBD1: Inflammatory bowel disease protein 1, ATG16L1: Autophagy-related 16-like 1, IRGM: Immunity-related GTPase family M protein, UC: Ulcerative colitis, IGF2: Insulin-like growth factor II, LOI: Loss of imprinting, PHLDA2: Pleckstrin homology like domain family A member 2