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Dependence receptors: new targets for cancer therapy
Dependence receptors are known to promote survival and positive signaling such as proliferation, migration, and differentiation when activated, but to actively trigger apoptosis when unbound to their ligand. Their abnormal regulation was shown to be an important feature of tumorigenesis, allowing ca...
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Published in: | EMBO molecular medicine 2021-11, Vol.13 (11), p.1-n/a |
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description | Dependence receptors are known to promote survival and positive signaling such as proliferation, migration, and differentiation when activated, but to actively trigger apoptosis when unbound to their ligand. Their abnormal regulation was shown to be an important feature of tumorigenesis, allowing cancer cells to escape apoptosis triggered by these receptors while promoting in parallel major aspects of tumorigenesis such as proliferation, angiogenesis, invasiveness, and chemoresistance. This involvement in multiple cancer hallmarks has raised interest in dependence receptors as targets for cancer therapy. Although additional studies remain necessary to fully understand the complexity of signaling pathways activated by these receptors and to target them efficiently, it is now clear that dependence receptors represent very exciting targets for future cancer treatment. This manuscript reviews current knowledge on the contribution of dependence receptors to cancer and highlights the potential for therapies that activate pro‐apoptotic functions of these proteins.
Graphical Abstract
Upon activation, dependence receptors promote survival, proliferation and migration but when unbound to their ligand, they trigger apoptosis. Here, F. Hollande & colleagues review the current knowledge on their contribution to cancer and discuss the therapeutic potential of targeting these receptors. |
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Graphical Abstract
Upon activation, dependence receptors promote survival, proliferation and migration but when unbound to their ligand, they trigger apoptosis. Here, F. Hollande & colleagues review the current knowledge on their contribution to cancer and discuss the therapeutic potential of targeting these receptors.</description><identifier>ISSN: 1757-4676</identifier><identifier>EISSN: 1757-4684</identifier><identifier>DOI: 10.15252/emmm.202114495</identifier><identifier>PMID: 34542930</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Angiogenesis ; Apoptosis ; Cancer ; cancer hallmarks ; Cancer therapies ; Chemoresistance ; EMBO03 ; EMBO07 ; EMBO37 ; Invasiveness ; Kinases ; Life Sciences ; Ligands ; Morphogenesis ; Proteins ; Review ; Signal transduction ; treatment resistance ; tumor progression ; Tumorigenesis</subject><ispartof>EMBO molecular medicine, 2021-11, Vol.13 (11), p.1-n/a</ispartof><rights>The Author(s) 2021</rights><rights>2021 The Authors Published under the terms of the CC BY 4.0 license</rights><rights>2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5905-ff14bcc7b187237c5d3239be5f081b4d0e02165763ab4917657ac6c816def4d63</citedby><cites>FETCH-LOGICAL-c5905-ff14bcc7b187237c5d3239be5f081b4d0e02165763ab4917657ac6c816def4d63</cites><orcidid>0000-0002-7046-8392 ; 0000-0001-6784-9496 ; 0000-0003-1743-5417 ; 0000-0002-8260-9711</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2594463274/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2594463274?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,11542,25732,27903,27904,36991,44569,46031,46455,53770,53772,74873</link.rule.ids><backlink>$$Uhttps://hal.science/hal-03456446$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Brisset, Morgan</creatorcontrib><creatorcontrib>Grandin, Mélodie</creatorcontrib><creatorcontrib>Bernet, Agnès</creatorcontrib><creatorcontrib>Mehlen, Patrick</creatorcontrib><creatorcontrib>Hollande, Frédéric</creatorcontrib><title>Dependence receptors: new targets for cancer therapy</title><title>EMBO molecular medicine</title><addtitle>EMBO Mol Med</addtitle><description>Dependence receptors are known to promote survival and positive signaling such as proliferation, migration, and differentiation when activated, but to actively trigger apoptosis when unbound to their ligand. Their abnormal regulation was shown to be an important feature of tumorigenesis, allowing cancer cells to escape apoptosis triggered by these receptors while promoting in parallel major aspects of tumorigenesis such as proliferation, angiogenesis, invasiveness, and chemoresistance. This involvement in multiple cancer hallmarks has raised interest in dependence receptors as targets for cancer therapy. Although additional studies remain necessary to fully understand the complexity of signaling pathways activated by these receptors and to target them efficiently, it is now clear that dependence receptors represent very exciting targets for future cancer treatment. This manuscript reviews current knowledge on the contribution of dependence receptors to cancer and highlights the potential for therapies that activate pro‐apoptotic functions of these proteins.
Graphical Abstract
Upon activation, dependence receptors promote survival, proliferation and migration but when unbound to their ligand, they trigger apoptosis. Here, F. Hollande & colleagues review the current knowledge on their contribution to cancer and discuss the therapeutic potential of targeting these receptors.</description><subject>Angiogenesis</subject><subject>Apoptosis</subject><subject>Cancer</subject><subject>cancer hallmarks</subject><subject>Cancer therapies</subject><subject>Chemoresistance</subject><subject>EMBO03</subject><subject>EMBO07</subject><subject>EMBO37</subject><subject>Invasiveness</subject><subject>Kinases</subject><subject>Life Sciences</subject><subject>Ligands</subject><subject>Morphogenesis</subject><subject>Proteins</subject><subject>Review</subject><subject>Signal transduction</subject><subject>treatment resistance</subject><subject>tumor progression</subject><subject>Tumorigenesis</subject><issn>1757-4676</issn><issn>1757-4684</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNqFkc1PGzEQxVdVq0KBc68r9dRDwN8fHCohSgEpEZf2bHntcbJRdr21N6D89zUsCqVSxcmj8Xu_Gc2rqs8YnWJOODmDrutOCSIYM6b5u-oQSy5nTCj2fl9LcVB9ynmNkOACq4_VAWWcEU3RYcW-wwC9h95BncDBMMaUz-seHurRpiWMuQ4x1c4WQarHFSQ77I6rD8FuMpw8v0fVrx9XPy9vZvO769vLi_nMcY34LATMGudkg5UkVDruKaG6AR6Qwg3zCMregktBbcM0lqW0TjiFhYfAvKBH1e3E9dGuzZDazqadibY1T42YlsamsXUbMMixgDxSSmvLvEINAiI8CgWqFSe2sL5NrGHbdOAd9GOym1fQ1z99uzLLeG8Ul5RrXQBfJ8DqH9vNxdw89lC5qmBM3OOi_fI8LMXfW8ijWcdt6sutDOG6aCiRrKjOJpVLMecEYY_FyDzFax7jNft4i-N8cjy0G9i9JTdXi8XibzOazLn4-iWkl6X-N-8PE7C1-g</recordid><startdate>20211108</startdate><enddate>20211108</enddate><creator>Brisset, Morgan</creator><creator>Grandin, Mélodie</creator><creator>Bernet, Agnès</creator><creator>Mehlen, Patrick</creator><creator>Hollande, Frédéric</creator><general>Nature Publishing Group UK</general><general>EMBO Press</general><general>Wiley Open Access</general><general>John Wiley and Sons Inc</general><general>Springer Nature</general><scope>C6C</scope><scope>24P</scope><scope>WIN</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</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>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>1XC</scope><scope>VOOES</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-7046-8392</orcidid><orcidid>https://orcid.org/0000-0001-6784-9496</orcidid><orcidid>https://orcid.org/0000-0003-1743-5417</orcidid><orcidid>https://orcid.org/0000-0002-8260-9711</orcidid></search><sort><creationdate>20211108</creationdate><title>Dependence receptors: new targets for cancer therapy</title><author>Brisset, Morgan ; 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Graphical Abstract
Upon activation, dependence receptors promote survival, proliferation and migration but when unbound to their ligand, they trigger apoptosis. Here, F. Hollande & colleagues review the current knowledge on their contribution to cancer and discuss the therapeutic potential of targeting these receptors.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>34542930</pmid><doi>10.15252/emmm.202114495</doi><tpages>3</tpages><orcidid>https://orcid.org/0000-0002-7046-8392</orcidid><orcidid>https://orcid.org/0000-0001-6784-9496</orcidid><orcidid>https://orcid.org/0000-0003-1743-5417</orcidid><orcidid>https://orcid.org/0000-0002-8260-9711</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Angiogenesis Apoptosis Cancer cancer hallmarks Cancer therapies Chemoresistance EMBO03 EMBO07 EMBO37 Invasiveness Kinases Life Sciences Ligands Morphogenesis Proteins Review Signal transduction treatment resistance tumor progression Tumorigenesis |
title | Dependence receptors: new targets for cancer therapy |
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