Table 1 Genes showed imprinting alteration in IBD and CRC-based studies

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

[40,41,42,43]

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]