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CXC chemokine receptor 4 (CXCR4) blockade in cancer treatment
CXC chemokine receptor type 4 (CXCR4) is a member of the G protein-coupled receptors (GPCRs) superfamily and is specific for CXC chemokine ligand 12 (CXCL12, also known as SDF-1), which makes CXCL12/CXCR4 axis. CXCR4 interacts with its ligand, triggering downstream signaling pathways that influence...
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| Published in: | Journal of cancer research and clinical oncology 2023-08, Vol.149 (10), p.7945-7968 |
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| container_title | Journal of cancer research and clinical oncology |
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| creator | Bao, Shunshun Darvishi, Mohammad H Amin, Ali Al-Haideri, Maysoon T. Patra, Indrajit Kashikova, Khadisha Ahmad, Irfan Alsaikhan, Fahad Al-qaim, Zahraa Haleem Al-Gazally, Moaed E. Kiasari, Bahman Abedi Tavakoli-Far, Bahareh Sidikov, Akmal A. Mustafa, Yasser Fakri Akhavan-Sigari, Reza |
| description | CXC chemokine receptor type 4 (CXCR4) is a member of the G protein-coupled receptors (GPCRs) superfamily and is specific for CXC chemokine ligand 12 (CXCL12, also known as SDF-1), which makes CXCL12/CXCR4 axis. CXCR4 interacts with its ligand, triggering downstream signaling pathways that influence cell proliferation chemotaxis, migration, and gene expression. The interaction also regulates physiological processes, including hematopoiesis, organogenesis, and tissue repair. Multiple evidence revealed that CXCL12/CXCR4 axis is implicated in several pathways involved in carcinogenesis and plays a key role in tumor growth, survival, angiogenesis, metastasis, and therapeutic resistance. Several CXCR4-targeting compounds have been discovered and used for preclinical and clinical cancer therapy, most of which have shown promising anti-tumor activity. In this review, we summarized the physiological signaling of the CXCL12/CXCR4 axis and described the role of this axis in tumor progression, and focused on the potential therapeutic options and strategies to block CXCR4. |
| doi_str_mv | 10.1007/s00432-022-04444-w |
| format | article |
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CXCR4 interacts with its ligand, triggering downstream signaling pathways that influence cell proliferation chemotaxis, migration, and gene expression. The interaction also regulates physiological processes, including hematopoiesis, organogenesis, and tissue repair. Multiple evidence revealed that CXCL12/CXCR4 axis is implicated in several pathways involved in carcinogenesis and plays a key role in tumor growth, survival, angiogenesis, metastasis, and therapeutic resistance. Several CXCR4-targeting compounds have been discovered and used for preclinical and clinical cancer therapy, most of which have shown promising anti-tumor activity. In this review, we summarized the physiological signaling of the CXCL12/CXCR4 axis and described the role of this axis in tumor progression, and focused on the potential therapeutic options and strategies to block CXCR4.</description><identifier>ISSN: 0171-5216</identifier><identifier>EISSN: 1432-1335</identifier><identifier>DOI: 10.1007/s00432-022-04444-w</identifier><identifier>PMID: 36905421</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Angiogenesis ; Antitumor agents ; Apoptosis ; Bone marrow ; Cancer Research ; Cancer therapies ; Carcinogenesis ; Cell growth ; Cell proliferation ; Chemokine CXCL12 - genetics ; Chemokine receptors ; Chemokines ; Chemotaxis ; CXC chemokines ; CXCL12 protein ; CXCR4 protein ; G protein-coupled receptors ; Gene expression ; Hematology ; Hemopoiesis ; HIV ; Human immunodeficiency virus ; Humans ; Hypertension ; Immune system ; Internal Medicine ; Kinases ; Leukemia ; Leukocyte migration ; Ligands ; Liver cancer ; Lung cancer ; Medical research ; Medicine ; Medicine & Public Health ; Metastases ; Metastasis ; Multiple myeloma ; Neoplasms - genetics ; Oncology ; Organogenesis ; Pharmacy ; Physiology ; Prostate ; Proteins ; Pulmonary arteries ; Receptors, CXCR4 - genetics ; Review ; SDF-1 protein ; Signal Transduction ; Stem cells ; Tumors ; Vascular endothelial growth factor</subject><ispartof>Journal of cancer research and clinical oncology, 2023-08, Vol.149 (10), p.7945-7968</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-c43750b8c9560d2fb673cff0d4fc175cc51883943d0b73700c9d90c2c8f248573</citedby><cites>FETCH-LOGICAL-c375t-c43750b8c9560d2fb673cff0d4fc175cc51883943d0b73700c9d90c2c8f248573</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36905421$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bao, Shunshun</creatorcontrib><creatorcontrib>Darvishi, Mohammad</creatorcontrib><creatorcontrib>H Amin, Ali</creatorcontrib><creatorcontrib>Al-Haideri, Maysoon T.</creatorcontrib><creatorcontrib>Patra, Indrajit</creatorcontrib><creatorcontrib>Kashikova, Khadisha</creatorcontrib><creatorcontrib>Ahmad, Irfan</creatorcontrib><creatorcontrib>Alsaikhan, Fahad</creatorcontrib><creatorcontrib>Al-qaim, Zahraa Haleem</creatorcontrib><creatorcontrib>Al-Gazally, Moaed E.</creatorcontrib><creatorcontrib>Kiasari, Bahman Abedi</creatorcontrib><creatorcontrib>Tavakoli-Far, Bahareh</creatorcontrib><creatorcontrib>Sidikov, Akmal A.</creatorcontrib><creatorcontrib>Mustafa, Yasser Fakri</creatorcontrib><creatorcontrib>Akhavan-Sigari, Reza</creatorcontrib><title>CXC chemokine receptor 4 (CXCR4) blockade in cancer treatment</title><title>Journal of cancer research and clinical oncology</title><addtitle>J Cancer Res Clin Oncol</addtitle><addtitle>J Cancer Res Clin Oncol</addtitle><description>CXC chemokine receptor type 4 (CXCR4) is a member of the G protein-coupled receptors (GPCRs) superfamily and is specific for CXC chemokine ligand 12 (CXCL12, also known as SDF-1), which makes CXCL12/CXCR4 axis. CXCR4 interacts with its ligand, triggering downstream signaling pathways that influence cell proliferation chemotaxis, migration, and gene expression. The interaction also regulates physiological processes, including hematopoiesis, organogenesis, and tissue repair. Multiple evidence revealed that CXCL12/CXCR4 axis is implicated in several pathways involved in carcinogenesis and plays a key role in tumor growth, survival, angiogenesis, metastasis, and therapeutic resistance. Several CXCR4-targeting compounds have been discovered and used for preclinical and clinical cancer therapy, most of which have shown promising anti-tumor activity. In this review, we summarized the physiological signaling of the CXCL12/CXCR4 axis and described the role of this axis in tumor progression, and focused on the potential therapeutic options and strategies to block CXCR4.</description><subject>Angiogenesis</subject><subject>Antitumor agents</subject><subject>Apoptosis</subject><subject>Bone marrow</subject><subject>Cancer Research</subject><subject>Cancer therapies</subject><subject>Carcinogenesis</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Chemokine CXCL12 - genetics</subject><subject>Chemokine receptors</subject><subject>Chemokines</subject><subject>Chemotaxis</subject><subject>CXC chemokines</subject><subject>CXCL12 protein</subject><subject>CXCR4 protein</subject><subject>G protein-coupled receptors</subject><subject>Gene expression</subject><subject>Hematology</subject><subject>Hemopoiesis</subject><subject>HIV</subject><subject>Human immunodeficiency virus</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Immune system</subject><subject>Internal Medicine</subject><subject>Kinases</subject><subject>Leukemia</subject><subject>Leukocyte migration</subject><subject>Ligands</subject><subject>Liver cancer</subject><subject>Lung cancer</subject><subject>Medical research</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Multiple myeloma</subject><subject>Neoplasms - genetics</subject><subject>Oncology</subject><subject>Organogenesis</subject><subject>Pharmacy</subject><subject>Physiology</subject><subject>Prostate</subject><subject>Proteins</subject><subject>Pulmonary arteries</subject><subject>Receptors, CXCR4 - genetics</subject><subject>Review</subject><subject>SDF-1 protein</subject><subject>Signal Transduction</subject><subject>Stem cells</subject><subject>Tumors</subject><subject>Vascular endothelial growth factor</subject><issn>0171-5216</issn><issn>1432-1335</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNp9kE1Lw0AQhhdRbK3-AQ8S8FIP0dmvbHLwIMEvKAii4G1JJhtN2yR1N6H4792aquDBgWGYnWfeHV5CjimcUwB14QAEZyEwn8JHuN4hY7p5opzLXTIGqmgoGY1G5MC5OfheKrZPRjxKQApGx-QyfUkDfDN1u6gaE1iDZtW1NhDB1E8exVmQL1tcZIUJqibArEFjg86arKtN0x2SvTJbOnO0rRPyfHP9lN6Fs4fb-_RqFiJXsgtR-AJ5jImMoGBlHimOZQmFKNGfhChpHPNE8AJyxRUAJkUCyDAumYil4hMyHXRXtn3vjet0XTk0y2XWmLZ3mqk4oiCYAI-e_kHnbW8bf51msWBRwpTgnmIDhbZ1zppSr2xVZ_ZDU9Abc_Vgrvbm6i9z9dovnWyl-7w2xc_Kt5se4APg_Kh5Nfb3739kPwFAvoFQ</recordid><startdate>20230801</startdate><enddate>20230801</enddate><creator>Bao, Shunshun</creator><creator>Darvishi, Mohammad</creator><creator>H Amin, Ali</creator><creator>Al-Haideri, Maysoon T.</creator><creator>Patra, Indrajit</creator><creator>Kashikova, Khadisha</creator><creator>Ahmad, Irfan</creator><creator>Alsaikhan, Fahad</creator><creator>Al-qaim, Zahraa Haleem</creator><creator>Al-Gazally, Moaed E.</creator><creator>Kiasari, Bahman Abedi</creator><creator>Tavakoli-Far, Bahareh</creator><creator>Sidikov, Akmal A.</creator><creator>Mustafa, Yasser Fakri</creator><creator>Akhavan-Sigari, Reza</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</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>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20230801</creationdate><title>CXC chemokine receptor 4 (CXCR4) blockade in cancer treatment</title><author>Bao, Shunshun ; Darvishi, Mohammad ; H Amin, Ali ; Al-Haideri, Maysoon T. ; Patra, Indrajit ; Kashikova, Khadisha ; Ahmad, Irfan ; Alsaikhan, Fahad ; Al-qaim, Zahraa Haleem ; Al-Gazally, Moaed E. ; Kiasari, Bahman Abedi ; Tavakoli-Far, Bahareh ; Sidikov, Akmal A. ; Mustafa, Yasser Fakri ; Akhavan-Sigari, Reza</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-c43750b8c9560d2fb673cff0d4fc175cc51883943d0b73700c9d90c2c8f248573</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Angiogenesis</topic><topic>Antitumor agents</topic><topic>Apoptosis</topic><topic>Bone marrow</topic><topic>Cancer Research</topic><topic>Cancer therapies</topic><topic>Carcinogenesis</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>Chemokine CXCL12 - 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Academic</collection><jtitle>Journal of cancer research and clinical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bao, Shunshun</au><au>Darvishi, Mohammad</au><au>H Amin, Ali</au><au>Al-Haideri, Maysoon T.</au><au>Patra, Indrajit</au><au>Kashikova, Khadisha</au><au>Ahmad, Irfan</au><au>Alsaikhan, Fahad</au><au>Al-qaim, Zahraa Haleem</au><au>Al-Gazally, Moaed E.</au><au>Kiasari, Bahman Abedi</au><au>Tavakoli-Far, Bahareh</au><au>Sidikov, Akmal A.</au><au>Mustafa, Yasser Fakri</au><au>Akhavan-Sigari, Reza</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CXC chemokine receptor 4 (CXCR4) blockade in cancer treatment</atitle><jtitle>Journal of cancer research and clinical oncology</jtitle><stitle>J Cancer Res Clin Oncol</stitle><addtitle>J Cancer Res Clin Oncol</addtitle><date>2023-08-01</date><risdate>2023</risdate><volume>149</volume><issue>10</issue><spage>7945</spage><epage>7968</epage><pages>7945-7968</pages><issn>0171-5216</issn><eissn>1432-1335</eissn><abstract>CXC chemokine receptor type 4 (CXCR4) is a member of the G protein-coupled receptors (GPCRs) superfamily and is specific for CXC chemokine ligand 12 (CXCL12, also known as SDF-1), which makes CXCL12/CXCR4 axis. CXCR4 interacts with its ligand, triggering downstream signaling pathways that influence cell proliferation chemotaxis, migration, and gene expression. The interaction also regulates physiological processes, including hematopoiesis, organogenesis, and tissue repair. Multiple evidence revealed that CXCL12/CXCR4 axis is implicated in several pathways involved in carcinogenesis and plays a key role in tumor growth, survival, angiogenesis, metastasis, and therapeutic resistance. Several CXCR4-targeting compounds have been discovered and used for preclinical and clinical cancer therapy, most of which have shown promising anti-tumor activity. In this review, we summarized the physiological signaling of the CXCL12/CXCR4 axis and described the role of this axis in tumor progression, and focused on the potential therapeutic options and strategies to block CXCR4.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>36905421</pmid><doi>10.1007/s00432-022-04444-w</doi><tpages>24</tpages></addata></record> |
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| subjects | Angiogenesis Antitumor agents Apoptosis Bone marrow Cancer Research Cancer therapies Carcinogenesis Cell growth Cell proliferation Chemokine CXCL12 - genetics Chemokine receptors Chemokines Chemotaxis CXC chemokines CXCL12 protein CXCR4 protein G protein-coupled receptors Gene expression Hematology Hemopoiesis HIV Human immunodeficiency virus Humans Hypertension Immune system Internal Medicine Kinases Leukemia Leukocyte migration Ligands Liver cancer Lung cancer Medical research Medicine Medicine & Public Health Metastases Metastasis Multiple myeloma Neoplasms - genetics Oncology Organogenesis Pharmacy Physiology Prostate Proteins Pulmonary arteries Receptors, CXCR4 - genetics Review SDF-1 protein Signal Transduction Stem cells Tumors Vascular endothelial growth factor |
| title | CXC chemokine receptor 4 (CXCR4) blockade in cancer treatment |
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