TY - JOUR
T1 - Partners in crime
T2 - The Lewis Y antigen and fucosyltransferase IV in Helicobacter pylori-induced gastric cancer
AU - Aziz, Faisal
AU - Khan, Imran
AU - Shukla, Shruti
AU - Dey, Debasish Kumar
AU - Yan, Qiu
AU - Chakraborty, Abhijit
AU - Yoshitomi, Hisae
AU - Hwang, Seung Kyu
AU - Sonwal, Sonam
AU - Lee, Hoomin
AU - Haldorai, Yuvaraj
AU - Xiao, Jianbo
AU - Huh, Yun Suk
AU - Bajpai, Vivek K.
AU - Han, Young Kyu
N1 - Publisher Copyright:
© 2021 Elsevier Inc.
PY - 2022/4
Y1 - 2022/4
N2 - Helicobacter pylori (H. pylori) is a major causative agent of chronic gastritis, gastric ulcer and gastric carcinoma. H. pylori cytotoxin associated antigen A (CagA) plays a crucial role in the development of gastric cancer. Gastric cancer is associated with glycosylation alterations in glycoproteins and glycolipids on the cell surface. H. pylori cytotoxin associated antigen A (CagA) plays a significant role in the progression of gastric cancer through post-translation modification of fucosylation to develop gastric cancer. The involvement of a variety of sugar antigens in the progression and development of gastric cancer has been investigated, including type II blood group antigens. Lewis Y (LeY) is overexpressed on the tumor cell surface either as a glycoprotein or glycolipid. LeY is a difucosylated oligosaccharide, which is catalyzed by fucosyltransferases such as FUT4 (α1,3). FUT4/LeY overexpression may serve as potential correlative biomarkers for the prognosis of gastric cancer. We discuss the various aspects of H. pylori in relation to fucosyltransferases (FUT1-FUT9) and its fucosylated Lewis antigens (LeY, LeX, LeA, and LeB) and gastric cancer. In this review, we summarize the carcinogenic effect of H. pylori CagA in association with LeY and its synthesis enzyme FUT4 in the development of gastric cancer as well as discuss its importance in the prognosis and its inhibition by combination therapy of anti-LeY antibody and celecoxib through MAPK signaling pathway preventing gastric carcinogenesis.
AB - Helicobacter pylori (H. pylori) is a major causative agent of chronic gastritis, gastric ulcer and gastric carcinoma. H. pylori cytotoxin associated antigen A (CagA) plays a crucial role in the development of gastric cancer. Gastric cancer is associated with glycosylation alterations in glycoproteins and glycolipids on the cell surface. H. pylori cytotoxin associated antigen A (CagA) plays a significant role in the progression of gastric cancer through post-translation modification of fucosylation to develop gastric cancer. The involvement of a variety of sugar antigens in the progression and development of gastric cancer has been investigated, including type II blood group antigens. Lewis Y (LeY) is overexpressed on the tumor cell surface either as a glycoprotein or glycolipid. LeY is a difucosylated oligosaccharide, which is catalyzed by fucosyltransferases such as FUT4 (α1,3). FUT4/LeY overexpression may serve as potential correlative biomarkers for the prognosis of gastric cancer. We discuss the various aspects of H. pylori in relation to fucosyltransferases (FUT1-FUT9) and its fucosylated Lewis antigens (LeY, LeX, LeA, and LeB) and gastric cancer. In this review, we summarize the carcinogenic effect of H. pylori CagA in association with LeY and its synthesis enzyme FUT4 in the development of gastric cancer as well as discuss its importance in the prognosis and its inhibition by combination therapy of anti-LeY antibody and celecoxib through MAPK signaling pathway preventing gastric carcinogenesis.
KW - Cytotoxin associated antigen A
KW - Fucosyltransferase IV
KW - Gastric cancer, Helicobacter pylori
KW - Lewis Y
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U2 - 10.1016/j.pharmthera.2021.107994
DO - 10.1016/j.pharmthera.2021.107994
M3 - Review article
C2 - 34571111
AN - SCOPUS:85116542537
SN - 0163-7258
VL - 232
JO - Pharmacology and Therapeutics
JF - Pharmacology and Therapeutics
M1 - 107994
ER -
