Role and Function of O-GlcNAcylation in Cancer
Cancer cells are able to reprogram their glucose metabolism and retain energy via glycolysis even under aerobic conditions. They activate the hexosamine biosynthetic pathway (HBP), and the complex interplay of O-linked N-acetylglucosaminylation (O-GlcNAcylation) via deprivation of nutrients or incre...
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| Veröffentlicht in: | Cancers 2021-10, Vol.13 (21), p.5365 |
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| creator | Lee, Jii Bum Pyo, Kyoung-Ho Kim, Hye Ryun |
| description | Cancer cells are able to reprogram their glucose metabolism and retain energy via glycolysis even under aerobic conditions. They activate the hexosamine biosynthetic pathway (HBP), and the complex interplay of O-linked N-acetylglucosaminylation (O-GlcNAcylation) via deprivation of nutrients or increase in cellular stress results in the proliferation, progression, and metastasis of cancer cells. Notably, cancer is one of the emerging diseases associated with O-GlcNAcylation. In this review, we summarize studies that delineate the role of O-GlcNAcylation in cancer, including its modulation in metastasis, function with receptor tyrosine kinases, and resistance to chemotherapeutic agents, such as cisplatin. In addition, we discuss the function of O-GlcNAcylation in eliciting immune responses associated with immune surveillance in the tumor microenvironment. O-GlcNAcylation is increasingly accepted as one of the key players involved in the activation and differentiation of T cells and macrophages. Finally, we discuss the prognostic role of O-GlcNAcylation and potential therapeutic agents such as O-linked β-N-acetylglucosamine-transferase inhibitors, which may help overcome the resistance mechanism associated with the reprogramming of glucose metabolism. |
| doi_str_mv | 10.3390/cancers13215365 |
| format | Article |
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They activate the hexosamine biosynthetic pathway (HBP), and the complex interplay of O-linked N-acetylglucosaminylation (O-GlcNAcylation) via deprivation of nutrients or increase in cellular stress results in the proliferation, progression, and metastasis of cancer cells. Notably, cancer is one of the emerging diseases associated with O-GlcNAcylation. In this review, we summarize studies that delineate the role of O-GlcNAcylation in cancer, including its modulation in metastasis, function with receptor tyrosine kinases, and resistance to chemotherapeutic agents, such as cisplatin. In addition, we discuss the function of O-GlcNAcylation in eliciting immune responses associated with immune surveillance in the tumor microenvironment. O-GlcNAcylation is increasingly accepted as one of the key players involved in the activation and differentiation of T cells and macrophages. Finally, we discuss the prognostic role of O-GlcNAcylation and potential therapeutic agents such as O-linked β-N-acetylglucosamine-transferase inhibitors, which may help overcome the resistance mechanism associated with the reprogramming of glucose metabolism.</description><identifier>ISSN: 2072-6694</identifier><identifier>EISSN: 2072-6694</identifier><identifier>DOI: 10.3390/cancers13215365</identifier><identifier>PMID: 34771527</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>Aerobic conditions ; Angiogenesis ; Cancer ; Cell activation ; Cell differentiation ; Cell proliferation ; Cellular stress response ; Chemotherapy ; Cisplatin ; DNA methylation ; Energy metabolism ; Enzymes ; Gene expression ; Glucose ; Glucose metabolism ; Glycolysis ; Homeostasis ; Hypotheses ; Immunosurveillance ; Immunotherapy ; Insulin ; Kinases ; Lymphocytes T ; Macrophages ; Metabolism ; Metastases ; Metastasis ; N-Acetylglucosamine ; Nutrients ; O-GlcNAcylation ; Phosphorylation ; Polypeptides ; Protein-tyrosine kinase receptors ; Proteins ; Review ; RNA polymerase ; Signal transduction ; Tumor cells ; Tumor microenvironment</subject><ispartof>Cancers, 2021-10, Vol.13 (21), p.5365</ispartof><rights>2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 by the authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c398t-6a0cf5ed7a789188784f18a195f78861a1e39b22670904ace86340eef23170633</citedby><cites>FETCH-LOGICAL-c398t-6a0cf5ed7a789188784f18a195f78861a1e39b22670904ace86340eef23170633</cites><orcidid>0000-0001-5608-3157</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8582477/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8582477/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids></links><search><creatorcontrib>Lee, Jii Bum</creatorcontrib><creatorcontrib>Pyo, Kyoung-Ho</creatorcontrib><creatorcontrib>Kim, Hye Ryun</creatorcontrib><title>Role and Function of O-GlcNAcylation in Cancer</title><title>Cancers</title><description>Cancer cells are able to reprogram their glucose metabolism and retain energy via glycolysis even under aerobic conditions. They activate the hexosamine biosynthetic pathway (HBP), and the complex interplay of O-linked N-acetylglucosaminylation (O-GlcNAcylation) via deprivation of nutrients or increase in cellular stress results in the proliferation, progression, and metastasis of cancer cells. Notably, cancer is one of the emerging diseases associated with O-GlcNAcylation. In this review, we summarize studies that delineate the role of O-GlcNAcylation in cancer, including its modulation in metastasis, function with receptor tyrosine kinases, and resistance to chemotherapeutic agents, such as cisplatin. In addition, we discuss the function of O-GlcNAcylation in eliciting immune responses associated with immune surveillance in the tumor microenvironment. O-GlcNAcylation is increasingly accepted as one of the key players involved in the activation and differentiation of T cells and macrophages. Finally, we discuss the prognostic role of O-GlcNAcylation and potential therapeutic agents such as O-linked β-N-acetylglucosamine-transferase inhibitors, which may help overcome the resistance mechanism associated with the reprogramming of glucose metabolism.</description><subject>Aerobic conditions</subject><subject>Angiogenesis</subject><subject>Cancer</subject><subject>Cell activation</subject><subject>Cell differentiation</subject><subject>Cell proliferation</subject><subject>Cellular stress response</subject><subject>Chemotherapy</subject><subject>Cisplatin</subject><subject>DNA methylation</subject><subject>Energy metabolism</subject><subject>Enzymes</subject><subject>Gene expression</subject><subject>Glucose</subject><subject>Glucose metabolism</subject><subject>Glycolysis</subject><subject>Homeostasis</subject><subject>Hypotheses</subject><subject>Immunosurveillance</subject><subject>Immunotherapy</subject><subject>Insulin</subject><subject>Kinases</subject><subject>Lymphocytes T</subject><subject>Macrophages</subject><subject>Metabolism</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>N-Acetylglucosamine</subject><subject>Nutrients</subject><subject>O-GlcNAcylation</subject><subject>Phosphorylation</subject><subject>Polypeptides</subject><subject>Protein-tyrosine kinase receptors</subject><subject>Proteins</subject><subject>Review</subject><subject>RNA polymerase</subject><subject>Signal transduction</subject><subject>Tumor cells</subject><subject>Tumor microenvironment</subject><issn>2072-6694</issn><issn>2072-6694</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkctLAzEQxoMottSevS548bJtHpvXRSjFVqFYED2HNJvVLdukJrtC_3vTB6KdywwzP775hgHgFsERIRKOjXbGhogIRpQwegH6GHKcMyaLyz91DwxjXMMUhCDO-DXokYJzRDHvg9Grb2ymXZnNOmfa2rvMV9kynzfmZWJ2jT60apdND8tuwFWlm2iHpzwA77PHt-lTvljOn6eTRW6IFG3ONDQVtSXXXEgkBBdFhYRGklZcCIY0skSuMGYcSlhoYwUjBbS2wskhZIQMwMNRd9utNrY01rVBN2ob6o0OO-V1rf5PXP2pPvy3ElTgdFwSuD8JBP_V2diqTR2NbRrtrO-iwlTyQtLkLaF3Z-jad8Gl8_YUg8kilYkaHykTfIzBVr9mEFT7d6izd5AfH_56hg</recordid><startdate>20211026</startdate><enddate>20211026</enddate><creator>Lee, Jii Bum</creator><creator>Pyo, Kyoung-Ho</creator><creator>Kim, Hye Ryun</creator><general>MDPI AG</general><general>MDPI</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-5608-3157</orcidid></search><sort><creationdate>20211026</creationdate><title>Role and Function of O-GlcNAcylation in Cancer</title><author>Lee, Jii Bum ; Pyo, Kyoung-Ho ; Kim, Hye Ryun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c398t-6a0cf5ed7a789188784f18a195f78861a1e39b22670904ace86340eef23170633</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Aerobic conditions</topic><topic>Angiogenesis</topic><topic>Cancer</topic><topic>Cell activation</topic><topic>Cell differentiation</topic><topic>Cell proliferation</topic><topic>Cellular stress response</topic><topic>Chemotherapy</topic><topic>Cisplatin</topic><topic>DNA methylation</topic><topic>Energy metabolism</topic><topic>Enzymes</topic><topic>Gene expression</topic><topic>Glucose</topic><topic>Glucose metabolism</topic><topic>Glycolysis</topic><topic>Homeostasis</topic><topic>Hypotheses</topic><topic>Immunosurveillance</topic><topic>Immunotherapy</topic><topic>Insulin</topic><topic>Kinases</topic><topic>Lymphocytes T</topic><topic>Macrophages</topic><topic>Metabolism</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>N-Acetylglucosamine</topic><topic>Nutrients</topic><topic>O-GlcNAcylation</topic><topic>Phosphorylation</topic><topic>Polypeptides</topic><topic>Protein-tyrosine kinase receptors</topic><topic>Proteins</topic><topic>Review</topic><topic>RNA polymerase</topic><topic>Signal transduction</topic><topic>Tumor cells</topic><topic>Tumor microenvironment</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Jii Bum</creatorcontrib><creatorcontrib>Pyo, Kyoung-Ho</creatorcontrib><creatorcontrib>Kim, Hye Ryun</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancers</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Jii Bum</au><au>Pyo, Kyoung-Ho</au><au>Kim, Hye Ryun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role and Function of O-GlcNAcylation in Cancer</atitle><jtitle>Cancers</jtitle><date>2021-10-26</date><risdate>2021</risdate><volume>13</volume><issue>21</issue><spage>5365</spage><pages>5365-</pages><issn>2072-6694</issn><eissn>2072-6694</eissn><abstract>Cancer cells are able to reprogram their glucose metabolism and retain energy via glycolysis even under aerobic conditions. They activate the hexosamine biosynthetic pathway (HBP), and the complex interplay of O-linked N-acetylglucosaminylation (O-GlcNAcylation) via deprivation of nutrients or increase in cellular stress results in the proliferation, progression, and metastasis of cancer cells. Notably, cancer is one of the emerging diseases associated with O-GlcNAcylation. In this review, we summarize studies that delineate the role of O-GlcNAcylation in cancer, including its modulation in metastasis, function with receptor tyrosine kinases, and resistance to chemotherapeutic agents, such as cisplatin. In addition, we discuss the function of O-GlcNAcylation in eliciting immune responses associated with immune surveillance in the tumor microenvironment. O-GlcNAcylation is increasingly accepted as one of the key players involved in the activation and differentiation of T cells and macrophages. Finally, we discuss the prognostic role of O-GlcNAcylation and potential therapeutic agents such as O-linked β-N-acetylglucosamine-transferase inhibitors, which may help overcome the resistance mechanism associated with the reprogramming of glucose metabolism.</abstract><cop>Basel</cop><pub>MDPI AG</pub><pmid>34771527</pmid><doi>10.3390/cancers13215365</doi><orcidid>https://orcid.org/0000-0001-5608-3157</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Aerobic conditions Angiogenesis Cancer Cell activation Cell differentiation Cell proliferation Cellular stress response Chemotherapy Cisplatin DNA methylation Energy metabolism Enzymes Gene expression Glucose Glucose metabolism Glycolysis Homeostasis Hypotheses Immunosurveillance Immunotherapy Insulin Kinases Lymphocytes T Macrophages Metabolism Metastases Metastasis N-Acetylglucosamine Nutrients O-GlcNAcylation Phosphorylation Polypeptides Protein-tyrosine kinase receptors Proteins Review RNA polymerase Signal transduction Tumor cells Tumor microenvironment |
| title | Role and Function of O-GlcNAcylation in Cancer |
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