Stimulation of triple negative breast cancer cell migration and metastases formation is prevented by chloroquine in a pre-irradiated mouse model.
Identifieur interne : 000204 ( PubMed/Corpus ); précédent : 000203; suivant : 000205Stimulation of triple negative breast cancer cell migration and metastases formation is prevented by chloroquine in a pre-irradiated mouse model.
Auteurs : Gina Bouchard ; Hélène Therriault ; Sameh Geha ; Yves Bérubé-Lauzière ; Rachel Bujold ; Caroline Saucier ; Benoit PaquetteSource :
- BMC cancer [ 1471-2407 ] ; 2016.
English descriptors
- KwdEn :
- Animals, Autophagy (drug effects), Cell Line, Tumor, Cell Movement (drug effects), Chloroquine (administration & dosage), Chloroquine (pharmacology), Cyclooxygenase 2 (metabolism), Female, Gene Expression Regulation, Neoplastic (drug effects), Humans, Interleukins (metabolism), Lung Neoplasms (drug therapy), Lung Neoplasms (secondary), MCF-7 Cells, Matrix Metalloproteinases (metabolism), Mice, Neoplasm Metastasis, Neoplastic Cells, Circulating (drug effects), Treatment Outcome, Triple Negative Breast Neoplasms (drug therapy), Triple Negative Breast Neoplasms (metabolism), Triple Negative Breast Neoplasms (radiotherapy), Xenograft Model Antitumor Assays.
- MESH :
- chemical , administration & dosage : Chloroquine.
- drug effects : Autophagy, Cell Movement, Gene Expression Regulation, Neoplastic, Neoplastic Cells, Circulating.
- drug therapy : Lung Neoplasms, Triple Negative Breast Neoplasms.
- chemical , metabolism : Cyclooxygenase 2, Interleukins, Matrix Metalloproteinases, Triple Negative Breast Neoplasms.
- chemical , pharmacology : Chloroquine.
- radiotherapy : Triple Negative Breast Neoplasms.
- secondary : Lung Neoplasms.
- Animals, Cell Line, Tumor, Female, Humans, MCF-7 Cells, Mice, Neoplasm Metastasis, Treatment Outcome, Xenograft Model Antitumor Assays.
Abstract
Some triple negative breast cancer (TNBC) patients are at higher risk of recurrence in the first three years after treatment. This rapid relapse has been suggested to be associated with inflammatory mediators induced by radiation in healthy tissues that stimulate cancer cell migration and metastasis formation. In this study, the ability of chloroquine (CQ) to inhibit radiation-stimulated development of metastasis was assessed.
DOI: 10.1186/s12885-016-2393-z
PubMed: 27282478
Links to Exploration step
pubmed:27282478Le document en format XML
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Benoit.Paquette@USherbrooke.ca.</nlm:affiliation></affiliation></author></analytic><series><title level="j">BMC cancer</title><idno type="eISSN">1471-2407</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Autophagy (drug effects)</term><term>Cell Line, Tumor</term><term>Cell Movement (drug effects)</term><term>Chloroquine (administration & dosage)</term><term>Chloroquine (pharmacology)</term><term>Cyclooxygenase 2 (metabolism)</term><term>Female</term><term>Gene Expression Regulation, Neoplastic (drug effects)</term><term>Humans</term><term>Interleukins (metabolism)</term><term>Lung Neoplasms (drug therapy)</term><term>Lung Neoplasms (secondary)</term><term>MCF-7 Cells</term><term>Matrix Metalloproteinases (metabolism)</term><term>Mice</term><term>Neoplasm Metastasis</term><term>Neoplastic Cells, Circulating (drug effects)</term><term>Treatment Outcome</term><term>Triple Negative Breast Neoplasms (drug therapy)</term><term>Triple Negative Breast Neoplasms (metabolism)</term><term>Triple Negative Breast Neoplasms (radiotherapy)</term><term>Xenograft Model Antitumor Assays</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term><term>Cell Movement</term><term>Gene Expression Regulation, Neoplastic</term><term>Neoplastic Cells, Circulating</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Lung Neoplasms</term><term>Triple Negative Breast Neoplasms</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cyclooxygenase 2</term><term>Interleukins</term><term>Matrix Metalloproteinases</term><term>Triple Negative Breast Neoplasms</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="radiotherapy" xml:lang="en"><term>Triple Negative Breast Neoplasms</term></keywords><keywords scheme="MESH" qualifier="secondary" xml:lang="en"><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line, Tumor</term><term>Female</term><term>Humans</term><term>MCF-7 Cells</term><term>Mice</term><term>Neoplasm Metastasis</term><term>Treatment Outcome</term><term>Xenograft Model Antitumor Assays</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Some triple negative breast cancer (TNBC) patients are at higher risk of recurrence in the first three years after treatment. This rapid relapse has been suggested to be associated with inflammatory mediators induced by radiation in healthy tissues that stimulate cancer cell migration and metastasis formation. In this study, the ability of chloroquine (CQ) to inhibit radiation-stimulated development of metastasis was assessed.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27282478</PMID><DateCompleted><Year>2017</Year><Month>10</Month><Day>09</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1471-2407</ISSN><JournalIssue CitedMedium="Internet"><Volume>16</Volume><PubDate><Year>2016</Year><Month>06</Month><Day>10</Day></PubDate></JournalIssue><Title>BMC cancer</Title><ISOAbbreviation>BMC Cancer</ISOAbbreviation></Journal><ArticleTitle>Stimulation of triple negative breast cancer cell migration and metastases formation is prevented by chloroquine in a pre-irradiated mouse model.</ArticleTitle><Pagination><MedlinePgn>361</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1186/s12885-016-2393-z</ELocationID><Abstract><AbstractText Label="BACKGROUND">Some triple negative breast cancer (TNBC) patients are at higher risk of recurrence in the first three years after treatment. This rapid relapse has been suggested to be associated with inflammatory mediators induced by radiation in healthy tissues that stimulate cancer cell migration and metastasis formation. In this study, the ability of chloroquine (CQ) to inhibit radiation-stimulated development of metastasis was assessed.</AbstractText><AbstractText Label="METHODS">The capacity of CQ to prevent radiation-enhancement of cancer cell invasion was assessed in vitro with the TNBC cell lines D2A1, 4T1 and MDA-MB-231 and the non-TNBC cell lines MC7-L1, and MCF-7. In Balb/c mice, a single mammary gland was irradiated with four daily doses of 6 Gy. After the last irradiation, irradiated and control mammary glands were implanted with D2A1 cells. Mice were treated with CQ (vehicle, 40 or 60 mg/kg) 3 h before each irradiation and then every 72 h for 3 weeks. Migration of D2A1 cells in the mammary gland, the number of circulating tumor cells and lung metastasis were quantified, and also the expression of some inflammatory mediators.</AbstractText><AbstractText Label="RESULTS">Irradiated fibroblasts have increased the invasiveness of the TNBC cell lines only, a stimulation that was prevented by CQ. On the other hand, invasiveness of the non-TNBC cell lines, which was not enhanced by irradiated fibroblasts, was also not significantly modified by CQ. In Balb/c mice, treatment with CQ prevented the stimulation of D2A1 TNBC cell migration in the pre-irradiated mammary gland, and reduced the number of circulating tumor cells and lung metastases. This protective effect of CQ was associated with a reduced expression of the inflammatory mediators interleukin-1β, interleukin-6, and cyclooxygenase-2, while the levels of matrix metalloproteinases-2 and -9 were not modified. CQ also promoted a blocking of autophagy.</AbstractText><AbstractText Label="CONCLUSION">CQ prevented radiation-enhancement of TNBC cell invasion and reduced the number of lung metastases in a mouse model.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bouchard</LastName><ForeName>Gina</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Centre for Research in Radiotherapy, Department of Nuclear Medicine and Radiobiology, Université de Sherbrooke, 3001, 12e Avenue Nord, Sherbrooke, Québec, J1H 5 N4, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Therriault</LastName><ForeName>Hélène</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Centre for Research in Radiotherapy, Department of Nuclear Medicine and Radiobiology, Université de Sherbrooke, 3001, 12e Avenue Nord, Sherbrooke, Québec, J1H 5 N4, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Geha</LastName><ForeName>Sameh</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Pathology, Centre Hospitalier Universitaire de Sherbrooke, Sherbrooke, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bérubé-Lauzière</LastName><ForeName>Yves</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Electrical and Computer Engineering, Centre d'imagerie moléculaire de Sherbrooke, Sherbrooke, Québec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bujold</LastName><ForeName>Rachel</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Centre for Research in Radiotherapy, Department of Nuclear Medicine and Radiobiology, Université de Sherbrooke, 3001, 12e Avenue Nord, Sherbrooke, Québec, J1H 5 N4, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Service of Radiation Oncology, Université de Sherbrooke, Sherbrooke, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Saucier</LastName><ForeName>Caroline</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Anatomy and Cellular Biology, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Paquette</LastName><ForeName>Benoit</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Centre for Research in Radiotherapy, Department of Nuclear Medicine and Radiobiology, Université de Sherbrooke, 3001, 12e Avenue Nord, Sherbrooke, Québec, J1H 5 N4, Canada. Benoit.Paquette@USherbrooke.ca.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>184671</GrantID><Agency>CIHR</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>06</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMC Cancer</MedlineTA><NlmUniqueID>100967800</NlmUniqueID><ISSNLinking>1471-2407</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007378">Interleukins</NameOfSubstance></Chemical><Chemical><RegistryNumber>886U3H6UFF</RegistryNumber><NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.99.1</RegistryNumber><NameOfSubstance UI="D051546">Cyclooxygenase 2</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.99.1</RegistryNumber><NameOfSubstance UI="C496540">PTGS2 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.24.-</RegistryNumber><NameOfSubstance UI="D020782">Matrix Metalloproteinases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002465" MajorTopicYN="N">Cell Movement</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002738" MajorTopicYN="N">Chloroquine</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="Y">administration & dosage</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051546" MajorTopicYN="N">Cyclooxygenase 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015972" MajorTopicYN="N">Gene Expression Regulation, Neoplastic</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007378" MajorTopicYN="N">Interleukins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008175" MajorTopicYN="N">Lung Neoplasms</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000556" MajorTopicYN="N">secondary</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D061986" MajorTopicYN="N">MCF-7 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020782" MajorTopicYN="N">Matrix Metalloproteinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009362" MajorTopicYN="N">Neoplasm Metastasis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009360" MajorTopicYN="N">Neoplastic Cells, Circulating</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D064726" MajorTopicYN="N">Triple Negative Breast Neoplasms</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000532" MajorTopicYN="Y">radiotherapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D023041" MajorTopicYN="N">Xenograft Model Antitumor Assays</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Chloroquine</Keyword><Keyword MajorTopicYN="Y">Inflammation</Keyword><Keyword MajorTopicYN="Y">Invasion</Keyword><Keyword MajorTopicYN="Y">Metastasis</Keyword><Keyword MajorTopicYN="Y">Radiation</Keyword><Keyword MajorTopicYN="Y">Triple negative breast cancer</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate 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