Partners in crime: The Lewis Y antigen and fucosyltransferase IV in Helicobacter pylori-induced gastric cancer
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 glycoprotein...
Gespeichert in:
| Veröffentlicht in: | Pharmacology & therapeutics (Oxford) 2022-04, Vol.232, p.107994-107994, Article 107994 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 107994 |
|---|---|
| container_issue | |
| container_start_page | 107994 |
| container_title | Pharmacology & therapeutics (Oxford) |
| container_volume | 232 |
| creator | Aziz, Faisal Khan, Imran Shukla, Shruti Dey, Debasish Kumar Yan, Qiu Chakraborty, Abhijit Yoshitomi, Hisae Hwang, Seung-Kyu Sonwal, Sonam Lee, Hoomin Haldorai, Yuvaraj Xiao, Jianbo Huh, Yun Suk Bajpai, Vivek K. Han, Young-Kyu |
| description | 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. |
| doi_str_mv | 10.1016/j.pharmthera.2021.107994 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2577460291</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0163725821001960</els_id><sourcerecordid>2577460291</sourcerecordid><originalsourceid>FETCH-LOGICAL-c440t-895d41e38b16080fdbafb9997bf112cb059b817d344eaf13cf36c4456ed16f003</originalsourceid><addsrcrecordid>eNqFkEtPAyEUhYnRaH38BcPSzVSYN-7UqG3SRBfV6IowcLE0U2YERtN_L02rLmVzEnLOPfd-CGFKxpTQ8nI57hfCrcICnBinJKXxu2Is30MjWlcsiZ7XfTSKkiVVWtRH6Nj7JSEkz0l6iI6yvKhofCNkn4QLFpzHxmLpzAqu8HwBeAZfxuM3LGww72CjKqwH2fl1G5ywXsdmD3j6sslNoDWya4QM4HC_bjtnEmPVIEHhd-GDMxJLYSW4U3SgRevhbKcn6Pn-bn47SWaPD9Pb61ki44YhqVmhcgpZ3dCS1ESrRuiGMVY1mtJUNqRgTU0rleU5CE0zqbMyJosSFC01IdkJutjO7V33MYAPfGW8hLYVFrrB87SoqrwkKaPRWm-t0nXeO9C8jxiEW3NK-IY2X_I_2nxDm29px-j5rmVoVqB-gz94o-Fma4B466cBx700EEEo40AGrjrzf8s3Cd6W6Q</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2577460291</pqid></control><display><type>article</type><title>Partners in crime: The Lewis Y antigen and fucosyltransferase IV in Helicobacter pylori-induced gastric cancer</title><source>MEDLINE</source><source>ScienceDirect Journals (5 years ago - present)</source><creator>Aziz, Faisal ; Khan, Imran ; Shukla, Shruti ; Dey, Debasish Kumar ; Yan, Qiu ; Chakraborty, Abhijit ; Yoshitomi, Hisae ; Hwang, Seung-Kyu ; Sonwal, Sonam ; Lee, Hoomin ; Haldorai, Yuvaraj ; Xiao, Jianbo ; Huh, Yun Suk ; Bajpai, Vivek K. ; Han, Young-Kyu</creator><creatorcontrib>Aziz, Faisal ; Khan, Imran ; Shukla, Shruti ; Dey, Debasish Kumar ; Yan, Qiu ; Chakraborty, Abhijit ; Yoshitomi, Hisae ; Hwang, Seung-Kyu ; Sonwal, Sonam ; Lee, Hoomin ; Haldorai, Yuvaraj ; Xiao, Jianbo ; Huh, Yun Suk ; Bajpai, Vivek K. ; Han, Young-Kyu</creatorcontrib><description>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.</description><identifier>ISSN: 0163-7258</identifier><identifier>EISSN: 1879-016X</identifier><identifier>DOI: 10.1016/j.pharmthera.2021.107994</identifier><identifier>PMID: 34571111</identifier><language>eng</language><publisher>England: Elsevier Inc</publisher><subject>Crime ; Cytotoxin associated antigen A ; Fucosyltransferase IV ; Fucosyltransferases - metabolism ; Gastric cancer, Helicobacter pylori ; Helicobacter Infections - complications ; Helicobacter pylori ; Humans ; Lewis Blood Group Antigens - metabolism ; Lewis Y ; Stomach Neoplasms - metabolism</subject><ispartof>Pharmacology & therapeutics (Oxford), 2022-04, Vol.232, p.107994-107994, Article 107994</ispartof><rights>2021 Elsevier Inc.</rights><rights>Copyright © 2021 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c440t-895d41e38b16080fdbafb9997bf112cb059b817d344eaf13cf36c4456ed16f003</citedby><cites>FETCH-LOGICAL-c440t-895d41e38b16080fdbafb9997bf112cb059b817d344eaf13cf36c4456ed16f003</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.pharmthera.2021.107994$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34571111$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aziz, Faisal</creatorcontrib><creatorcontrib>Khan, Imran</creatorcontrib><creatorcontrib>Shukla, Shruti</creatorcontrib><creatorcontrib>Dey, Debasish Kumar</creatorcontrib><creatorcontrib>Yan, Qiu</creatorcontrib><creatorcontrib>Chakraborty, Abhijit</creatorcontrib><creatorcontrib>Yoshitomi, Hisae</creatorcontrib><creatorcontrib>Hwang, Seung-Kyu</creatorcontrib><creatorcontrib>Sonwal, Sonam</creatorcontrib><creatorcontrib>Lee, Hoomin</creatorcontrib><creatorcontrib>Haldorai, Yuvaraj</creatorcontrib><creatorcontrib>Xiao, Jianbo</creatorcontrib><creatorcontrib>Huh, Yun Suk</creatorcontrib><creatorcontrib>Bajpai, Vivek K.</creatorcontrib><creatorcontrib>Han, Young-Kyu</creatorcontrib><title>Partners in crime: The Lewis Y antigen and fucosyltransferase IV in Helicobacter pylori-induced gastric cancer</title><title>Pharmacology & therapeutics (Oxford)</title><addtitle>Pharmacol Ther</addtitle><description>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.</description><subject>Crime</subject><subject>Cytotoxin associated antigen A</subject><subject>Fucosyltransferase IV</subject><subject>Fucosyltransferases - metabolism</subject><subject>Gastric cancer, Helicobacter pylori</subject><subject>Helicobacter Infections - complications</subject><subject>Helicobacter pylori</subject><subject>Humans</subject><subject>Lewis Blood Group Antigens - metabolism</subject><subject>Lewis Y</subject><subject>Stomach Neoplasms - metabolism</subject><issn>0163-7258</issn><issn>1879-016X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEtPAyEUhYnRaH38BcPSzVSYN-7UqG3SRBfV6IowcLE0U2YERtN_L02rLmVzEnLOPfd-CGFKxpTQ8nI57hfCrcICnBinJKXxu2Is30MjWlcsiZ7XfTSKkiVVWtRH6Nj7JSEkz0l6iI6yvKhofCNkn4QLFpzHxmLpzAqu8HwBeAZfxuM3LGww72CjKqwH2fl1G5ywXsdmD3j6sslNoDWya4QM4HC_bjtnEmPVIEHhd-GDMxJLYSW4U3SgRevhbKcn6Pn-bn47SWaPD9Pb61ki44YhqVmhcgpZ3dCS1ESrRuiGMVY1mtJUNqRgTU0rleU5CE0zqbMyJosSFC01IdkJutjO7V33MYAPfGW8hLYVFrrB87SoqrwkKaPRWm-t0nXeO9C8jxiEW3NK-IY2X_I_2nxDm29px-j5rmVoVqB-gz94o-Fma4B466cBx700EEEo40AGrjrzf8s3Cd6W6Q</recordid><startdate>202204</startdate><enddate>202204</enddate><creator>Aziz, Faisal</creator><creator>Khan, Imran</creator><creator>Shukla, Shruti</creator><creator>Dey, Debasish Kumar</creator><creator>Yan, Qiu</creator><creator>Chakraborty, Abhijit</creator><creator>Yoshitomi, Hisae</creator><creator>Hwang, Seung-Kyu</creator><creator>Sonwal, Sonam</creator><creator>Lee, Hoomin</creator><creator>Haldorai, Yuvaraj</creator><creator>Xiao, Jianbo</creator><creator>Huh, Yun Suk</creator><creator>Bajpai, Vivek K.</creator><creator>Han, Young-Kyu</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>202204</creationdate><title>Partners in crime: The Lewis Y antigen and fucosyltransferase IV in Helicobacter pylori-induced gastric cancer</title><author>Aziz, Faisal ; Khan, Imran ; Shukla, Shruti ; Dey, Debasish Kumar ; Yan, Qiu ; Chakraborty, Abhijit ; Yoshitomi, Hisae ; Hwang, Seung-Kyu ; Sonwal, Sonam ; Lee, Hoomin ; Haldorai, Yuvaraj ; Xiao, Jianbo ; Huh, Yun Suk ; Bajpai, Vivek K. ; Han, Young-Kyu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c440t-895d41e38b16080fdbafb9997bf112cb059b817d344eaf13cf36c4456ed16f003</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Crime</topic><topic>Cytotoxin associated antigen A</topic><topic>Fucosyltransferase IV</topic><topic>Fucosyltransferases - metabolism</topic><topic>Gastric cancer, Helicobacter pylori</topic><topic>Helicobacter Infections - complications</topic><topic>Helicobacter pylori</topic><topic>Humans</topic><topic>Lewis Blood Group Antigens - metabolism</topic><topic>Lewis Y</topic><topic>Stomach Neoplasms - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aziz, Faisal</creatorcontrib><creatorcontrib>Khan, Imran</creatorcontrib><creatorcontrib>Shukla, Shruti</creatorcontrib><creatorcontrib>Dey, Debasish Kumar</creatorcontrib><creatorcontrib>Yan, Qiu</creatorcontrib><creatorcontrib>Chakraborty, Abhijit</creatorcontrib><creatorcontrib>Yoshitomi, Hisae</creatorcontrib><creatorcontrib>Hwang, Seung-Kyu</creatorcontrib><creatorcontrib>Sonwal, Sonam</creatorcontrib><creatorcontrib>Lee, Hoomin</creatorcontrib><creatorcontrib>Haldorai, Yuvaraj</creatorcontrib><creatorcontrib>Xiao, Jianbo</creatorcontrib><creatorcontrib>Huh, Yun Suk</creatorcontrib><creatorcontrib>Bajpai, Vivek K.</creatorcontrib><creatorcontrib>Han, Young-Kyu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Pharmacology & therapeutics (Oxford)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aziz, Faisal</au><au>Khan, Imran</au><au>Shukla, Shruti</au><au>Dey, Debasish Kumar</au><au>Yan, Qiu</au><au>Chakraborty, Abhijit</au><au>Yoshitomi, Hisae</au><au>Hwang, Seung-Kyu</au><au>Sonwal, Sonam</au><au>Lee, Hoomin</au><au>Haldorai, Yuvaraj</au><au>Xiao, Jianbo</au><au>Huh, Yun Suk</au><au>Bajpai, Vivek K.</au><au>Han, Young-Kyu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Partners in crime: The Lewis Y antigen and fucosyltransferase IV in Helicobacter pylori-induced gastric cancer</atitle><jtitle>Pharmacology & therapeutics (Oxford)</jtitle><addtitle>Pharmacol Ther</addtitle><date>2022-04</date><risdate>2022</risdate><volume>232</volume><spage>107994</spage><epage>107994</epage><pages>107994-107994</pages><artnum>107994</artnum><issn>0163-7258</issn><eissn>1879-016X</eissn><abstract>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.</abstract><cop>England</cop><pub>Elsevier Inc</pub><pmid>34571111</pmid><doi>10.1016/j.pharmthera.2021.107994</doi><tpages>1</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0163-7258 |
| ispartof | Pharmacology & therapeutics (Oxford), 2022-04, Vol.232, p.107994-107994, Article 107994 |
| issn | 0163-7258 1879-016X |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2577460291 |
| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Crime Cytotoxin associated antigen A Fucosyltransferase IV Fucosyltransferases - metabolism Gastric cancer, Helicobacter pylori Helicobacter Infections - complications Helicobacter pylori Humans Lewis Blood Group Antigens - metabolism Lewis Y Stomach Neoplasms - metabolism |
| title | Partners in crime: The Lewis Y antigen and fucosyltransferase IV in Helicobacter pylori-induced gastric cancer |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-11T13%3A46%3A03IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Partners%20in%20crime:%20The%20Lewis%20Y%20antigen%20and%20fucosyltransferase%20IV%20in%20Helicobacter%20pylori-induced%20gastric%20cancer&rft.jtitle=Pharmacology%20&%20therapeutics%20(Oxford)&rft.au=Aziz,%20Faisal&rft.date=2022-04&rft.volume=232&rft.spage=107994&rft.epage=107994&rft.pages=107994-107994&rft.artnum=107994&rft.issn=0163-7258&rft.eissn=1879-016X&rft_id=info:doi/10.1016/j.pharmthera.2021.107994&rft_dat=%3Cproquest_cross%3E2577460291%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2577460291&rft_id=info:pmid/34571111&rft_els_id=S0163725821001960&rfr_iscdi=true |