CCL20 triggered by chemotherapy hinders the therapeutic efficacy of breast cancer
Chemotherapeutic resistance in triple-negative breast cancer (TNBC) has brought great challenges to the improvement of patient survival. The mechanisms of taxane chemoresistance in TNBC have not been well investigated. Our results illustrated C-C motif chemokine ligand 20 (CCL20) was significantly e...
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| creator | Chen, Weilong Qin, Yuanyuan Wang, Dong Zhou, Lei Liu, Yin Chen, Sheng Yin, Liang Xiao, Yaoxing Yao, Xiao-Hong Yang, Xiaoli Ma, Wei Chen, Weifeng He, Xueyan Zhang, Lixing Yang, Qifeng Bian, Xiuwu Shao, Zhi-Ming Liu, Suling |
| description | Chemotherapeutic resistance in triple-negative breast cancer (TNBC) has brought great challenges to the improvement of patient survival. The mechanisms of taxane chemoresistance in TNBC have not been well investigated. Our results illustrated C-C motif chemokine ligand 20 (CCL20) was significantly elevated during taxane-containing chemotherapy in breast cancer patients with nonpathologic complete response. Furthermore, CCL20 promoted the self-renewal and maintenance of breast cancer stem cells (BCSCs) or breast cancer stem-like cells through protein kinase Cζ (PKCζ) or p38 mitogen-activated protein kinase (MAPK)-mediated activation of p65 nuclear factor kappa B (NF-κB) pathway, significantly increasing the frequency and taxane resistance of BCSCs. Moreover, CCL20-promoted NF-κB activation increased ATP-binding cassette subfamily B member 1 (ABCB1)/multidrug resistance 1 (MDR1) expression, leading to the extracellular efflux of taxane. These results suggested that chemotherapy-induced CCL20 mediated chemoresistance via up-regulating ABCB1. In addition, NF-κB activation increased CCL20 expression, forming a positive feedback loop between NF-κB and CCL20 pathways, which provides sustained impetus for chemoresistance in breast cancer cells. Our results suggest that CCL20 can be a novel predictive marker for taxane response, and the blockade of CCL20 or its downstream pathway might reverse the taxane resistance in breast cancer patients. |
| doi_str_mv | 10.1371/journal.pbio.2005869 |
| format | Article |
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The mechanisms of taxane chemoresistance in TNBC have not been well investigated. Our results illustrated C-C motif chemokine ligand 20 (CCL20) was significantly elevated during taxane-containing chemotherapy in breast cancer patients with nonpathologic complete response. Furthermore, CCL20 promoted the self-renewal and maintenance of breast cancer stem cells (BCSCs) or breast cancer stem-like cells through protein kinase Cζ (PKCζ) or p38 mitogen-activated protein kinase (MAPK)-mediated activation of p65 nuclear factor kappa B (NF-κB) pathway, significantly increasing the frequency and taxane resistance of BCSCs. Moreover, CCL20-promoted NF-κB activation increased ATP-binding cassette subfamily B member 1 (ABCB1)/multidrug resistance 1 (MDR1) expression, leading to the extracellular efflux of taxane. These results suggested that chemotherapy-induced CCL20 mediated chemoresistance via up-regulating ABCB1. In addition, NF-κB activation increased CCL20 expression, forming a positive feedback loop between NF-κB and CCL20 pathways, which provides sustained impetus for chemoresistance in breast cancer cells. Our results suggest that CCL20 can be a novel predictive marker for taxane response, and the blockade of CCL20 or its downstream pathway might reverse the taxane resistance in breast cancer patients.</description><identifier>ISSN: 1545-7885</identifier><identifier>ISSN: 1544-9173</identifier><identifier>EISSN: 1545-7885</identifier><identifier>DOI: 10.1371/journal.pbio.2005869</identifier><identifier>PMID: 30052635</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Activation ; Apoptosis ; Biology and Life Sciences ; Breast cancer ; Cancer ; CCL20 protein ; Cell self-renewal ; Chemoresistance ; Chemotherapy ; Chronic illnesses ; Cytokines ; Drug therapy ; Efflux ; Feedback loops ; Gene expression ; Glycoproteins ; Kinases ; Laboratories ; Leukemia ; Life sciences ; Lymphoma ; MAP kinase ; MDR1 protein ; Medicine and Health Sciences ; Multidrug resistance ; NF-κB protein ; Oncology ; P-Glycoprotein ; Pathology ; Patient outcomes ; Patients ; Positive feedback ; Protein kinase ; Protein kinase C ; Proteins ; Research and Analysis Methods ; Senescence ; Stem cells ; Surgery ; Taxanes</subject><ispartof>PLoS biology, 2018-07, Vol.16 (7), p.e2005869-e2005869</ispartof><rights>COPYRIGHT 2018 Public Library of Science</rights><rights>2018 Chen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2018 Chen et al 2018 Chen et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c695t-c333ed71aae95713f27c0bde3d34bfcbe391361c6ed67a6685293b2479fd80573</citedby><cites>FETCH-LOGICAL-c695t-c333ed71aae95713f27c0bde3d34bfcbe391361c6ed67a6685293b2479fd80573</cites><orcidid>0000-0002-0475-0242</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/PMC6082578/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6082578/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,729,782,786,866,887,2106,2932,23875,27933,27934,53800,53802</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30052635$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Eaves, Connie</contributor><creatorcontrib>Chen, Weilong</creatorcontrib><creatorcontrib>Qin, Yuanyuan</creatorcontrib><creatorcontrib>Wang, Dong</creatorcontrib><creatorcontrib>Zhou, Lei</creatorcontrib><creatorcontrib>Liu, Yin</creatorcontrib><creatorcontrib>Chen, Sheng</creatorcontrib><creatorcontrib>Yin, Liang</creatorcontrib><creatorcontrib>Xiao, Yaoxing</creatorcontrib><creatorcontrib>Yao, Xiao-Hong</creatorcontrib><creatorcontrib>Yang, Xiaoli</creatorcontrib><creatorcontrib>Ma, Wei</creatorcontrib><creatorcontrib>Chen, Weifeng</creatorcontrib><creatorcontrib>He, Xueyan</creatorcontrib><creatorcontrib>Zhang, Lixing</creatorcontrib><creatorcontrib>Yang, Qifeng</creatorcontrib><creatorcontrib>Bian, Xiuwu</creatorcontrib><creatorcontrib>Shao, Zhi-Ming</creatorcontrib><creatorcontrib>Liu, Suling</creatorcontrib><title>CCL20 triggered by chemotherapy hinders the therapeutic efficacy of breast cancer</title><title>PLoS biology</title><addtitle>PLoS Biol</addtitle><description>Chemotherapeutic resistance in triple-negative breast cancer (TNBC) has brought great challenges to the improvement of patient survival. The mechanisms of taxane chemoresistance in TNBC have not been well investigated. Our results illustrated C-C motif chemokine ligand 20 (CCL20) was significantly elevated during taxane-containing chemotherapy in breast cancer patients with nonpathologic complete response. Furthermore, CCL20 promoted the self-renewal and maintenance of breast cancer stem cells (BCSCs) or breast cancer stem-like cells through protein kinase Cζ (PKCζ) or p38 mitogen-activated protein kinase (MAPK)-mediated activation of p65 nuclear factor kappa B (NF-κB) pathway, significantly increasing the frequency and taxane resistance of BCSCs. Moreover, CCL20-promoted NF-κB activation increased ATP-binding cassette subfamily B member 1 (ABCB1)/multidrug resistance 1 (MDR1) expression, leading to the extracellular efflux of taxane. These results suggested that chemotherapy-induced CCL20 mediated chemoresistance via up-regulating ABCB1. In addition, NF-κB activation increased CCL20 expression, forming a positive feedback loop between NF-κB and CCL20 pathways, which provides sustained impetus for chemoresistance in breast cancer cells. Our results suggest that CCL20 can be a novel predictive marker for taxane response, and the blockade of CCL20 or its downstream pathway might reverse the taxane resistance in breast cancer patients.</description><subject>Activation</subject><subject>Apoptosis</subject><subject>Biology and Life Sciences</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>CCL20 protein</subject><subject>Cell self-renewal</subject><subject>Chemoresistance</subject><subject>Chemotherapy</subject><subject>Chronic illnesses</subject><subject>Cytokines</subject><subject>Drug therapy</subject><subject>Efflux</subject><subject>Feedback loops</subject><subject>Gene expression</subject><subject>Glycoproteins</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Leukemia</subject><subject>Life sciences</subject><subject>Lymphoma</subject><subject>MAP kinase</subject><subject>MDR1 protein</subject><subject>Medicine and Health Sciences</subject><subject>Multidrug resistance</subject><subject>NF-κB protein</subject><subject>Oncology</subject><subject>P-Glycoprotein</subject><subject>Pathology</subject><subject>Patient outcomes</subject><subject>Patients</subject><subject>Positive feedback</subject><subject>Protein kinase</subject><subject>Protein kinase C</subject><subject>Proteins</subject><subject>Research and Analysis Methods</subject><subject>Senescence</subject><subject>Stem cells</subject><subject>Surgery</subject><subject>Taxanes</subject><issn>1545-7885</issn><issn>1544-9173</issn><issn>1545-7885</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqVksuO0zAUhiMEYobCGyCIxAYWLb7Etw3SqOJSqWLEdWs5znHqURoXO0H07XFpZjRFswB5Yfv4O799jv-ieIrRAlOBX1-FMfamW-xqHxYEISa5ulecY1axuZCS3b-1PisepXSFECGKyIfFGc044ZSdF5-WyzVB5RB920KEpqz3pd3ANgwbiGa3Lze-byCmMu_LYwzGwdsSnPPW2H0ZXFlHMGkorektxMfFA2e6BE-meVZ8e_f26_LDfH35frW8WM8tV2yYW0opNAIbA4oJTB0RFtUN0IZWtbM1UIUpx5ZDw4XhXDKiaE0qoVwjERN0Vjw_6u66kPTUjaQJkopWnCqUidWRaIK50rvotybudTBe_wmE2GoTcy0daCm5QLZhjoGspDIKG8GZkrWocX6iy1pvptvGeguNhX6IpjsRPT3p_Ua34afmSBImZBZ4OQnE8GOENOitTxa6zvQQxsO7hWSSklz1rHjxF3p3dRPVmlyA713I99qDqL5gleQUZVNkanEHlUcDW29DD87n-EnCq5OEzAzwa2jNmJJeffn8H-zHf2cvv5-y1ZG1MaQUwd30GSN9MP91Q_TB_Hoyf057dvuPbpKu3U5_AydJ_YA</recordid><startdate>20180727</startdate><enddate>20180727</enddate><creator>Chen, 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triggered by chemotherapy hinders the therapeutic efficacy of breast cancer</title><author>Chen, Weilong ; Qin, Yuanyuan ; Wang, Dong ; Zhou, Lei ; Liu, Yin ; Chen, Sheng ; Yin, Liang ; Xiao, Yaoxing ; Yao, Xiao-Hong ; Yang, Xiaoli ; Ma, Wei ; Chen, Weifeng ; He, Xueyan ; Zhang, Lixing ; Yang, Qifeng ; Bian, Xiuwu ; Shao, Zhi-Ming ; Liu, Suling</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c695t-c333ed71aae95713f27c0bde3d34bfcbe391361c6ed67a6685293b2479fd80573</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Activation</topic><topic>Apoptosis</topic><topic>Biology and Life Sciences</topic><topic>Breast cancer</topic><topic>Cancer</topic><topic>CCL20 protein</topic><topic>Cell self-renewal</topic><topic>Chemoresistance</topic><topic>Chemotherapy</topic><topic>Chronic illnesses</topic><topic>Cytokines</topic><topic>Drug therapy</topic><topic>Efflux</topic><topic>Feedback loops</topic><topic>Gene expression</topic><topic>Glycoproteins</topic><topic>Kinases</topic><topic>Laboratories</topic><topic>Leukemia</topic><topic>Life sciences</topic><topic>Lymphoma</topic><topic>MAP kinase</topic><topic>MDR1 protein</topic><topic>Medicine and Health Sciences</topic><topic>Multidrug resistance</topic><topic>NF-κB protein</topic><topic>Oncology</topic><topic>P-Glycoprotein</topic><topic>Pathology</topic><topic>Patient outcomes</topic><topic>Patients</topic><topic>Positive feedback</topic><topic>Protein kinase</topic><topic>Protein kinase C</topic><topic>Proteins</topic><topic>Research and Analysis Methods</topic><topic>Senescence</topic><topic>Stem cells</topic><topic>Surgery</topic><topic>Taxanes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Weilong</creatorcontrib><creatorcontrib>Qin, Yuanyuan</creatorcontrib><creatorcontrib>Wang, Dong</creatorcontrib><creatorcontrib>Zhou, 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Weilong</au><au>Qin, Yuanyuan</au><au>Wang, Dong</au><au>Zhou, Lei</au><au>Liu, Yin</au><au>Chen, Sheng</au><au>Yin, Liang</au><au>Xiao, Yaoxing</au><au>Yao, Xiao-Hong</au><au>Yang, Xiaoli</au><au>Ma, Wei</au><au>Chen, Weifeng</au><au>He, Xueyan</au><au>Zhang, Lixing</au><au>Yang, Qifeng</au><au>Bian, Xiuwu</au><au>Shao, Zhi-Ming</au><au>Liu, Suling</au><au>Eaves, Connie</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CCL20 triggered by chemotherapy hinders the therapeutic efficacy of breast cancer</atitle><jtitle>PLoS biology</jtitle><addtitle>PLoS Biol</addtitle><date>2018-07-27</date><risdate>2018</risdate><volume>16</volume><issue>7</issue><spage>e2005869</spage><epage>e2005869</epage><pages>e2005869-e2005869</pages><issn>1545-7885</issn><issn>1544-9173</issn><eissn>1545-7885</eissn><abstract>Chemotherapeutic resistance in triple-negative breast cancer (TNBC) has brought great challenges to the improvement of patient survival. The mechanisms of taxane chemoresistance in TNBC have not been well investigated. Our results illustrated C-C motif chemokine ligand 20 (CCL20) was significantly elevated during taxane-containing chemotherapy in breast cancer patients with nonpathologic complete response. Furthermore, CCL20 promoted the self-renewal and maintenance of breast cancer stem cells (BCSCs) or breast cancer stem-like cells through protein kinase Cζ (PKCζ) or p38 mitogen-activated protein kinase (MAPK)-mediated activation of p65 nuclear factor kappa B (NF-κB) pathway, significantly increasing the frequency and taxane resistance of BCSCs. Moreover, CCL20-promoted NF-κB activation increased ATP-binding cassette subfamily B member 1 (ABCB1)/multidrug resistance 1 (MDR1) expression, leading to the extracellular efflux of taxane. These results suggested that chemotherapy-induced CCL20 mediated chemoresistance via up-regulating ABCB1. In addition, NF-κB activation increased CCL20 expression, forming a positive feedback loop between NF-κB and CCL20 pathways, which provides sustained impetus for chemoresistance in breast cancer cells. Our results suggest that CCL20 can be a novel predictive marker for taxane response, and the blockade of CCL20 or its downstream pathway might reverse the taxane resistance in breast cancer patients.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>30052635</pmid><doi>10.1371/journal.pbio.2005869</doi><orcidid>https://orcid.org/0000-0002-0475-0242</orcidid><oa>free_for_read</oa></addata></record> |
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| source | Public Library of Science (PLoS) Journals Open Access; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Activation Apoptosis Biology and Life Sciences Breast cancer Cancer CCL20 protein Cell self-renewal Chemoresistance Chemotherapy Chronic illnesses Cytokines Drug therapy Efflux Feedback loops Gene expression Glycoproteins Kinases Laboratories Leukemia Life sciences Lymphoma MAP kinase MDR1 protein Medicine and Health Sciences Multidrug resistance NF-κB protein Oncology P-Glycoprotein Pathology Patient outcomes Patients Positive feedback Protein kinase Protein kinase C Proteins Research and Analysis Methods Senescence Stem cells Surgery Taxanes |
| title | CCL20 triggered by chemotherapy hinders the therapeutic efficacy of breast cancer |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-01T05%3A54%3A27IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=CCL20%20triggered%20by%20chemotherapy%20hinders%20the%20therapeutic%20efficacy%20of%20breast%20cancer&rft.jtitle=PLoS%20biology&rft.au=Chen,%20Weilong&rft.date=2018-07-27&rft.volume=16&rft.issue=7&rft.spage=e2005869&rft.epage=e2005869&rft.pages=e2005869-e2005869&rft.issn=1545-7885&rft.eissn=1545-7885&rft_id=info:doi/10.1371/journal.pbio.2005869&rft_dat=%3Cgale_plos_%3EA548630200%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2089346390&rft_id=info:pmid/30052635&rft_galeid=A548630200&rft_doaj_id=oai_doaj_org_article_88670cd5f5e8489a91a76598b7b11aaf&rfr_iscdi=true |