Table 1.

Main contributions of the receptor for advanced glycation end products axis to gastric carcinogenesis

Mechanism	Impact in gastric carcinogenesis	Year of publication	Ref.
RAGE overexpression	Promote tumor growth, migration and highly invasive phenotypes	2002	Kuniyasu et al[93]
	Association with high invasive histopathological grade, and poor overall survival	2015	Wang et al[94]
RAGE polymorphisms
rs2070600	Association with increased risk of GC and highly invasive features	2008	Gu et al[138]
	Association with increased risk of GC	2017	Li et al[139]
rs184003	Association with decrease risk of GC	2017	Li et al[139]
RAGE activation
HMGB1	Association with advance pT stage	2021	Zhou and Yang[74]
	Promotes GC cell proliferation and migration	2021	Tang et al[77]
	Support cancer cell survival and chemoresistance	2015	Zhang et al[86]
	Association to higher TNM stage, lymph node metastasis, and depth of invasion	2021	Zhou et al[105]
	Increased macrophage infiltration	2007	Akaike et al[103]
	Enhance tumor angiogenesis through induction of IL-8	2017	Chung et al[110]
	Promotes EMT activation and increased cell motility/invasiveness	2015	Chung et al[111]
	Promote GC progression via EMT	2020	Jin et al[104]
AGEs	Upregulation of pro-tumoral mediators	2017	Deng et al[127]
S100 proteins	Enhance tumor cell proliferation and migration	2021	You et al[80]
	Induced migration and invasion in GC cells	2013	Kwon et al[117]
	Promoting progression and invasion in GC cells	2007	Yong and Moon[118]
	Immunosuppressive RAGE-mediated effects	2013	Wang et al[119]
	Dysregulation of apoptotic factors	2020	Shabani et al[120]

AGE: Advanced glycation end products; EMT: Epithelial-to-mesenchymal transition; GC: Gastric cancer; HMGB1: High mobility group box 1; IL: Interleukin; RAGE: Receptor for advanced glycation end products.