The A2b adenosine receptor antagonist PSB-603 promotes oxidative phosphorylation and ROS production in colorectal cancer cells via adenosine receptor-independent mechanism.
Identifieur interne : 001596 ( PubMed/Checkpoint ); précédent : 001595; suivant : 001597The A2b adenosine receptor antagonist PSB-603 promotes oxidative phosphorylation and ROS production in colorectal cancer cells via adenosine receptor-independent mechanism.
Auteurs : Christina M Lck [Australie] ; James Ryall [Australie] ; Laura M. Failla [Australie] ; Janine L. Coates [Australie] ; Jean-Marc Pascussi [France] ; Joan K. Heath [Australie] ; Gregory Stewart [Australie] ; Frédéric Hollande [Australie]Source :
- Cancer letters [ 1872-7980 ] ; 2016.
Descripteurs français
- KwdFr :
- AMP cyclique (métabolisme), Antagonistes des récepteurs A2 à l'adénosine (pharmacologie), Antinéoplasiques (pharmacologie), Composés organiques du platine (pharmacologie), Consommation d'oxygène (), Endocytose (), Espèces réactives de l'oxygène (métabolisme), Facteurs temps, Fluorouracil (pharmacologie), Humains, Interférence par ARN, Lignée cellulaire tumorale, Mitochondries (), Mitochondries (métabolisme), Mort cellulaire (), Oxydoréduction, Phosphorylation oxydative (), Protocoles de polychimiothérapie antinéoplasique (pharmacologie), Relation dose-effet des médicaments, Récepteur A2B à l'adénosine (), Récepteur A2B à l'adénosine (génétique), Récepteur A2B à l'adénosine (métabolisme), Stress oxydatif (), Sulfonamides (pharmacologie), Transduction du signal (), Transfection, Tumeurs colorectales (anatomopathologie), Tumeurs colorectales (génétique), Tumeurs colorectales (métabolisme), Tumeurs colorectales (traitement médicamenteux), Xanthines (pharmacologie).
- MESH :
- anatomopathologie : Tumeurs colorectales.
- génétique : Récepteur A2B à l'adénosine, Tumeurs colorectales.
- métabolisme : AMP cyclique, Espèces réactives de l'oxygène, Mitochondries, Récepteur A2B à l'adénosine, Tumeurs colorectales.
- pharmacologie : Antagonistes des récepteurs A2 à l'adénosine, Antinéoplasiques, Composés organiques du platine, Fluorouracil, Protocoles de polychimiothérapie antinéoplasique, Sulfonamides, Xanthines.
- traitement médicamenteux : Tumeurs colorectales.
- Consommation d'oxygène, Endocytose, Facteurs temps, Humains, Interférence par ARN, Lignée cellulaire tumorale, Mitochondries, Mort cellulaire, Oxydoréduction, Phosphorylation oxydative, Relation dose-effet des médicaments, Récepteur A2B à l'adénosine, Stress oxydatif, Transduction du signal, Transfection.
English descriptors
- KwdEn :
- Adenosine A2 Receptor Antagonists (pharmacology), Antineoplastic Agents (pharmacology), Antineoplastic Combined Chemotherapy Protocols (pharmacology), Cell Death (drug effects), Cell Line, Tumor, Colorectal Neoplasms (drug therapy), Colorectal Neoplasms (genetics), Colorectal Neoplasms (metabolism), Colorectal Neoplasms (pathology), Cyclic AMP (metabolism), Dose-Response Relationship, Drug, Endocytosis (drug effects), Fluorouracil (pharmacology), Humans, Mitochondria (drug effects), Mitochondria (metabolism), Organoplatinum Compounds (pharmacology), Oxidation-Reduction, Oxidative Phosphorylation (drug effects), Oxidative Stress (drug effects), Oxygen Consumption (drug effects), RNA Interference, Reactive Oxygen Species (metabolism), Receptor, Adenosine A2B (drug effects), Receptor, Adenosine A2B (genetics), Receptor, Adenosine A2B (metabolism), Signal Transduction (drug effects), Sulfonamides (pharmacology), Time Factors, Transfection, Xanthines (pharmacology).
- MESH :
- chemical , drug effects : Receptor, Adenosine A2B.
- chemical , genetics : Receptor, Adenosine A2B.
- chemical , metabolism : Cyclic AMP, Reactive Oxygen Species, Receptor, Adenosine A2B.
- chemical , pharmacology : Adenosine A2 Receptor Antagonists, Antineoplastic Agents, Fluorouracil, Organoplatinum Compounds, Sulfonamides, Xanthines.
- drug effects : Cell Death, Endocytosis, Mitochondria, Oxidative Phosphorylation, Oxidative Stress, Oxygen Consumption, Signal Transduction.
- drug therapy : Colorectal Neoplasms.
- genetics : Colorectal Neoplasms.
- metabolism : Colorectal Neoplasms, Mitochondria.
- pathology : Colorectal Neoplasms.
- pharmacology : Antineoplastic Combined Chemotherapy Protocols.
- Cell Line, Tumor, Dose-Response Relationship, Drug, Humans, Oxidation-Reduction, RNA Interference, Time Factors, Transfection.
Abstract
Adenosine is a multifaceted regulator of tumor progression. It modulates immune cell activity as well as acting directly on tumor cells. The A2b adenosine receptor (A2b-AR) is thought to be an important mediator of these effects. In this study we sought to analyze the contribution of the A2b-AR to the behavior of colorectal cancer cells.
DOI: 10.1016/j.canlet.2016.09.018
PubMed: 27693637
Affiliations:
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pubmed:27693637Le document en format XML
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Heath</name><affiliation wicri:level="4"><nlm:affiliation>The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia; Department of Medical Biology, The University of Melbourne, Parkville, Victoria 3010, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia; Department of Medical Biology, The University of Melbourne, Parkville, Victoria 3010</wicri:regionArea><orgName type="university">Université de Melbourne</orgName><placeName><settlement type="city">Melbourne</settlement><region type="état">Victoria (État)</region></placeName></affiliation></author><author><name sortKey="Stewart, Gregory" sort="Stewart, Gregory" uniqKey="Stewart G" first="Gregory" last="Stewart">Gregory Stewart</name><affiliation wicri:level="1"><nlm:affiliation>Drug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Victoria 3052, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Drug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Victoria 3052</wicri:regionArea><wicri:noRegion>Victoria 3052</wicri:noRegion></affiliation></author><author><name sortKey="Hollande, Frederic" sort="Hollande, Frederic" uniqKey="Hollande F" first="Frédéric" last="Hollande">Frédéric Hollande</name><affiliation wicri:level="4"><nlm:affiliation>Department of Pathology, The University of Melbourne, Parkville, Victoria 3010, Australia. Electronic address: frederic.hollande@unimelb.edu.au.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Pathology, The University of Melbourne, Parkville, Victoria 3010</wicri:regionArea><orgName type="university">Université de Melbourne</orgName><placeName><settlement type="city">Melbourne</settlement><region type="état">Victoria (État)</region></placeName></affiliation></author></analytic><series><title level="j">Cancer letters</title><idno type="eISSN">1872-7980</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenosine A2 Receptor Antagonists (pharmacology)</term><term>Antineoplastic Agents (pharmacology)</term><term>Antineoplastic Combined Chemotherapy Protocols (pharmacology)</term><term>Cell Death (drug effects)</term><term>Cell Line, Tumor</term><term>Colorectal Neoplasms (drug therapy)</term><term>Colorectal Neoplasms (genetics)</term><term>Colorectal Neoplasms (metabolism)</term><term>Colorectal Neoplasms (pathology)</term><term>Cyclic AMP (metabolism)</term><term>Dose-Response Relationship, Drug</term><term>Endocytosis (drug effects)</term><term>Fluorouracil (pharmacology)</term><term>Humans</term><term>Mitochondria (drug effects)</term><term>Mitochondria (metabolism)</term><term>Organoplatinum Compounds (pharmacology)</term><term>Oxidation-Reduction</term><term>Oxidative Phosphorylation (drug effects)</term><term>Oxidative Stress (drug effects)</term><term>Oxygen Consumption (drug effects)</term><term>RNA Interference</term><term>Reactive Oxygen Species (metabolism)</term><term>Receptor, Adenosine A2B (drug effects)</term><term>Receptor, Adenosine A2B (genetics)</term><term>Receptor, Adenosine A2B (metabolism)</term><term>Signal Transduction (drug effects)</term><term>Sulfonamides (pharmacology)</term><term>Time Factors</term><term>Transfection</term><term>Xanthines (pharmacology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>AMP cyclique (métabolisme)</term><term>Antagonistes des récepteurs A2 à l'adénosine (pharmacologie)</term><term>Antinéoplasiques (pharmacologie)</term><term>Composés organiques du platine (pharmacologie)</term><term>Consommation d'oxygène ()</term><term>Endocytose ()</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Facteurs temps</term><term>Fluorouracil (pharmacologie)</term><term>Humains</term><term>Interférence par ARN</term><term>Lignée cellulaire tumorale</term><term>Mitochondries ()</term><term>Mitochondries (métabolisme)</term><term>Mort cellulaire ()</term><term>Oxydoréduction</term><term>Phosphorylation oxydative ()</term><term>Protocoles de polychimiothérapie antinéoplasique (pharmacologie)</term><term>Relation dose-effet des médicaments</term><term>Récepteur A2B à l'adénosine ()</term><term>Récepteur A2B à l'adénosine (génétique)</term><term>Récepteur A2B à l'adénosine (métabolisme)</term><term>Stress oxydatif ()</term><term>Sulfonamides (pharmacologie)</term><term>Transduction du signal ()</term><term>Transfection</term><term>Tumeurs colorectales (anatomopathologie)</term><term>Tumeurs colorectales (génétique)</term><term>Tumeurs colorectales (métabolisme)</term><term>Tumeurs colorectales (traitement médicamenteux)</term><term>Xanthines (pharmacologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Receptor, Adenosine A2B</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Receptor, Adenosine A2B</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cyclic AMP</term><term>Reactive Oxygen Species</term><term>Receptor, Adenosine A2B</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Adenosine A2 Receptor Antagonists</term><term>Antineoplastic Agents</term><term>Fluorouracil</term><term>Organoplatinum Compounds</term><term>Sulfonamides</term><term>Xanthines</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Tumeurs colorectales</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Death</term><term>Endocytosis</term><term>Mitochondria</term><term>Oxidative Phosphorylation</term><term>Oxidative Stress</term><term>Oxygen Consumption</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Colorectal Neoplasms</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Colorectal Neoplasms</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Récepteur A2B à l'adénosine</term><term>Tumeurs colorectales</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Colorectal Neoplasms</term><term>Mitochondria</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>AMP cyclique</term><term>Espèces réactives de l'oxygène</term><term>Mitochondries</term><term>Récepteur A2B à l'adénosine</term><term>Tumeurs colorectales</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Colorectal Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antagonistes des récepteurs A2 à l'adénosine</term><term>Antinéoplasiques</term><term>Composés organiques du platine</term><term>Fluorouracil</term><term>Protocoles de polychimiothérapie antinéoplasique</term><term>Sulfonamides</term><term>Xanthines</term></keywords><keywords scheme="MESH" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Combined Chemotherapy Protocols</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Tumeurs colorectales</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>Dose-Response Relationship, Drug</term><term>Humans</term><term>Oxidation-Reduction</term><term>RNA Interference</term><term>Time Factors</term><term>Transfection</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Consommation d'oxygène</term><term>Endocytose</term><term>Facteurs temps</term><term>Humains</term><term>Interférence par ARN</term><term>Lignée cellulaire tumorale</term><term>Mitochondries</term><term>Mort cellulaire</term><term>Oxydoréduction</term><term>Phosphorylation oxydative</term><term>Relation dose-effet des médicaments</term><term>Récepteur A2B à l'adénosine</term><term>Stress oxydatif</term><term>Transduction du signal</term><term>Transfection</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Adenosine is a multifaceted regulator of tumor progression. It modulates immune cell activity as well as acting directly on tumor cells. The A2b adenosine receptor (A2b-AR) is thought to be an important mediator of these effects. In this study we sought to analyze the contribution of the A2b-AR to the behavior of colorectal cancer cells.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27693637</PMID><DateCreated><Year>2016</Year><Month>10</Month><Day>03</Day></DateCreated><DateCompleted><Year>2017</Year><Month>07</Month><Day>24</Day></DateCompleted><DateRevised><Year>2017</Year><Month>10</Month><Day>29</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-7980</ISSN><JournalIssue CitedMedium="Internet"><Volume>383</Volume><Issue>1</Issue><PubDate><Year>2016</Year><Month>12</Month><Day>01</Day></PubDate></JournalIssue><Title>Cancer letters</Title><ISOAbbreviation>Cancer Lett.</ISOAbbreviation></Journal><ArticleTitle>The A2b adenosine receptor antagonist PSB-603 promotes oxidative phosphorylation and ROS production in colorectal cancer cells via adenosine receptor-independent mechanism.</ArticleTitle><Pagination><MedlinePgn>135-143</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0304-3835(16)30560-2</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.canlet.2016.09.018</ELocationID><Abstract><AbstractText Label="PURPOSE">Adenosine is a multifaceted regulator of tumor progression. It modulates immune cell activity as well as acting directly on tumor cells. The A2b adenosine receptor (A2b-AR) is thought to be an important mediator of these effects. In this study we sought to analyze the contribution of the A2b-AR to the behavior of colorectal cancer cells.</AbstractText><AbstractText Label="PRINCIPAL RESULTS">The A2b-AR antagonist PSB-603 changed cellular redox state without affecting cellular viability. Quantification of cellular bioenergetics demonstrated that PSB-603 increased basal oxygen consumption rates, indicative of enhanced mitochondrial oxidative phosphorylation. Unexpectedly, pharmacological and genetic approaches to antagonize AR-related signalling of PSB-603 did not abolish the response, suggesting that it was AR-independent. PSB-603 also induced acute increases in reactive oxygen species, and PSB-603 synergized with chemotherapy treatment to increase colorectal cancer cell death, consistent with the known link between cellular metabolism and chemotherapy response.</AbstractText><AbstractText Label="MAJOR CONCLUSIONS">PSB-603 alters cellular metabolism in colorectal cancer cells and increases their sensitivity to chemotherapy. Although requiring more mechanistic insight into its A2b-AR-independent activity, our results show that PSB-603 may have clinical value as an anti-colorectal cancer therapeutic.</AbstractText><CopyrightInformation>Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mølck</LastName><ForeName>Christina</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Pathology, The University of Melbourne, Parkville, Victoria 3010, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ryall</LastName><ForeName>James</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Physiology, The University of Melbourne, Parkville, Victoria 3010, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Failla</LastName><ForeName>Laura M</ForeName><Initials>LM</Initials><AffiliationInfo><Affiliation>Department of Pathology, The University of Melbourne, Parkville, Victoria 3010, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Coates</LastName><ForeName>Janine L</ForeName><Initials>JL</Initials><AffiliationInfo><Affiliation>The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pascussi</LastName><ForeName>Jean-Marc</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>CNRS, UMR-5203, Institut de Génomique Fonctionnelle, F-34000 Montpellier, France; INSERM, U1191, F-34000 Montpellier, France; Universités de Montpellier, F-34000 Montpellier, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Heath</LastName><ForeName>Joan K</ForeName><Initials>JK</Initials><AffiliationInfo><Affiliation>The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia; Department of Medical Biology, The University of Melbourne, Parkville, Victoria 3010, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stewart</LastName><ForeName>Gregory</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Drug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Victoria 3052, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hollande</LastName><ForeName>Frédéric</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Pathology, The University of Melbourne, Parkville, Victoria 3010, Australia. Electronic address: frederic.hollande@unimelb.edu.au.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>09</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Cancer Lett</MedlineTA><NlmUniqueID>7600053</NlmUniqueID><ISSNLinking>0304-3835</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D058917">Adenosine A2 Receptor Antagonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000970">Antineoplastic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009944">Organoplatinum 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species</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>06</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>09</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>09</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>10</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>7</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>10</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27693637</ArticleId><ArticleId IdType="pii">S0304-3835(16)30560-2</ArticleId><ArticleId IdType="doi">10.1016/j.canlet.2016.09.018</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Australie</li><li>France</li></country><region><li>Victoria (État)</li></region><settlement><li>Melbourne</li></settlement><orgName><li>Université de Melbourne</li></orgName></list><tree><country name="Australie"><region name="Victoria (État)"><name sortKey="M Lck, Christina" sort="M Lck, Christina" uniqKey="M Lck C" first="Christina" last="M Lck">Christina M Lck</name></region><name sortKey="Coates, Janine L" sort="Coates, Janine L" uniqKey="Coates J" first="Janine L" last="Coates">Janine L. Coates</name><name sortKey="Failla, Laura M" sort="Failla, Laura M" uniqKey="Failla L" first="Laura M" last="Failla">Laura M. Failla</name><name sortKey="Heath, Joan K" sort="Heath, Joan K" uniqKey="Heath J" first="Joan K" last="Heath">Joan K. Heath</name><name sortKey="Hollande, Frederic" sort="Hollande, Frederic" uniqKey="Hollande F" first="Frédéric" last="Hollande">Frédéric Hollande</name><name sortKey="Ryall, James" sort="Ryall, James" uniqKey="Ryall J" first="James" last="Ryall">James Ryall</name><name sortKey="Stewart, Gregory" sort="Stewart, Gregory" uniqKey="Stewart G" first="Gregory" last="Stewart">Gregory Stewart</name></country><country name="France"><noRegion><name sortKey="Pascussi, Jean Marc" sort="Pascussi, Jean Marc" uniqKey="Pascussi J" first="Jean-Marc" last="Pascussi">Jean-Marc Pascussi</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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