WillowV1, Main, Corpus, bibRecord, 001061

Analysis of tumour- and stroma-supplied proteolytic networks reveals a brain-metastasis-promoting role for cathepsin S.

Identifieur interne : 001061 ( Main/Corpus ); précédent : 001060; suivant : 001062

Analysis of tumour- and stroma-supplied proteolytic networks reveals a brain-metastasis-promoting role for cathepsin S.

Auteurs : Lisa Sevenich ; Robert L. Bowman ; Steven D. Mason ; Daniela F. Quail ; Franck Rapaport ; Benelita T. Elie ; Edi Brogi ; Priscilla K. Brastianos ; William C. Hahn ; Leslie J. Holsinger ; Joan Massagué ; Christina S. Leslie ; Johanna A. Joyce

Source :

Nature cell biology [ 1476-4679 ] ; 2014.

RBID : pubmed:25086747

English descriptors

KwdEn :
- Animals (MeSH), Antineoplastic Agents (pharmacology), Biomarkers, Tumor (metabolism), Blood-Brain Barrier (pathology), Bone Neoplasms (enzymology), Bone Neoplasms (mortality), Bone Neoplasms (secondary), Brain Neoplasms (enzymology), Brain Neoplasms (mortality), Brain Neoplasms (secondary), Breast Neoplasms (enzymology), Breast Neoplasms (mortality), Breast Neoplasms (pathology), Cathepsins (antagonists & inhibitors), Cathepsins (physiology), Cell Line, Tumor (MeSH), Cell Movement (MeSH), Cystatins (metabolism), Disease-Free Survival (MeSH), Female (MeSH), Humans (MeSH), Kaplan-Meier Estimate (MeSH), Lung Neoplasms (enzymology), Lung Neoplasms (mortality), Lung Neoplasms (secondary), Mice (MeSH), Mice, Inbred NOD (MeSH), Mice, Knockout (MeSH), Mice, Nude (MeSH), Mice, SCID (MeSH), Organ Specificity (MeSH), Protease Inhibitors (pharmacology), Proteolysis (MeSH), Serpins (metabolism), Tight Junction Proteins (metabolism), Tumor Microenvironment (MeSH), Xenograft Model Antitumor Assays (MeSH).
MESH :
- chemical , antagonists & inhibitors : Cathepsins.
- chemical , metabolism : Biomarkers, Tumor, Cystatins, Serpins, Tight Junction Proteins.
- chemical , pharmacology : Antineoplastic Agents, Protease Inhibitors.
- enzymology : Bone Neoplasms, Brain Neoplasms, Breast Neoplasms, Lung Neoplasms.
- mortality : Bone Neoplasms, Brain Neoplasms, Breast Neoplasms, Lung Neoplasms.
- pathology : Blood-Brain Barrier, Breast Neoplasms.
- chemical , physiology : Cathepsins.
- secondary : Bone Neoplasms, Brain Neoplasms, Lung Neoplasms.
- Animals, Cell Line, Tumor, Cell Movement, Disease-Free Survival, Female, Humans, Kaplan-Meier Estimate, Mice, Mice, Inbred NOD, Mice, Knockout, Mice, Nude, Mice, SCID, Organ Specificity, Proteolysis, Tumor Microenvironment, Xenograft Model Antitumor Assays.

Abstract

Metastasis remains the most common cause of death in most cancers, with limited therapies for combating disseminated disease. While the primary tumour microenvironment is an important regulator of cancer progression, it is less well understood how different tissue environments influence metastasis. We analysed tumour-stroma interactions that modulate organ tropism of brain, bone and lung metastasis in xenograft models. We identified a number of potential modulators of site-specific metastasis, including cathepsin S as a regulator of breast-to-brain metastasis. High cathepsin S expression at the primary site correlated with decreased brain metastasis-free survival in breast cancer patients. Both macrophages and tumour cells produce cathepsin S, and only the combined depletion significantly reduced brain metastasis in vivo. Cathepsin S specifically mediates blood-brain barrier transmigration through proteolytic processing of the junctional adhesion molecule, JAM-B. Pharmacological inhibition of cathepsin S significantly reduced experimental brain metastasis, supporting its consideration as a therapeutic target for this disease.

DOI: 10.1038/ncb3011
PubMed: 25086747
PubMed Central: PMC4249762

Links to Exploration step

pubmed:25086747

Le document en format XML

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<author><name sortKey="Joyce, Johanna A" sort="Joyce, Johanna A" uniqKey="Joyce J" first="Johanna A" last="Joyce">Johanna A. Joyce</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Analysis of tumour- and stroma-supplied proteolytic networks reveals a brain-metastasis-promoting role for cathepsin S.</title>
<author><name sortKey="Sevenich, Lisa" sort="Sevenich, Lisa" uniqKey="Sevenich L" first="Lisa" last="Sevenich">Lisa Sevenich</name>
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</affiliation>
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<author><name sortKey="Bowman, Robert L" sort="Bowman, Robert L" uniqKey="Bowman R" first="Robert L" last="Bowman">Robert L. Bowman</name>
<affiliation><nlm:affiliation>1] Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA [2].</nlm:affiliation>
</affiliation>
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<author><name sortKey="Mason, Steven D" sort="Mason, Steven D" uniqKey="Mason S" first="Steven D" last="Mason">Steven D. Mason</name>
<affiliation><nlm:affiliation>1] Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA [2].</nlm:affiliation>
</affiliation>
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<author><name sortKey="Quail, Daniela F" sort="Quail, Daniela F" uniqKey="Quail D" first="Daniela F" last="Quail">Daniela F. Quail</name>
<affiliation><nlm:affiliation>Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.</nlm:affiliation>
</affiliation>
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<author><name sortKey="Rapaport, Franck" sort="Rapaport, Franck" uniqKey="Rapaport F" first="Franck" last="Rapaport">Franck Rapaport</name>
<affiliation><nlm:affiliation>Computational Biology Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.</nlm:affiliation>
</affiliation>
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<author><name sortKey="Elie, Benelita T" sort="Elie, Benelita T" uniqKey="Elie B" first="Benelita T" last="Elie">Benelita T. Elie</name>
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</affiliation>
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<author><name sortKey="Brogi, Edi" sort="Brogi, Edi" uniqKey="Brogi E" first="Edi" last="Brogi">Edi Brogi</name>
<affiliation><nlm:affiliation>Pathology Department, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Brastianos, Priscilla K" sort="Brastianos, Priscilla K" uniqKey="Brastianos P" first="Priscilla K" last="Brastianos">Priscilla K. Brastianos</name>
<affiliation><nlm:affiliation>1] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [2] Division of Hematology/Oncology, Massachusetts General Hospital, Boston, Massachusetts 02214, USA.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Hahn, William C" sort="Hahn, William C" uniqKey="Hahn W" first="William C" last="Hahn">William C. Hahn</name>
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<author><name sortKey="Holsinger, Leslie J" sort="Holsinger, Leslie J" uniqKey="Holsinger L" first="Leslie J" last="Holsinger">Leslie J. Holsinger</name>
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</affiliation>
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<author><name sortKey="Massague, Joan" sort="Massague, Joan" uniqKey="Massague J" first="Joan" last="Massagué">Joan Massagué</name>
<affiliation><nlm:affiliation>1] Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA [2] Brain Tumor Center, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA [3] Metastasis Research Center, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.</nlm:affiliation>
</affiliation>
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<author><name sortKey="Leslie, Christina S" sort="Leslie, Christina S" uniqKey="Leslie C" first="Christina S" last="Leslie">Christina S. Leslie</name>
<affiliation><nlm:affiliation>Computational Biology Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Joyce, Johanna A" sort="Joyce, Johanna A" uniqKey="Joyce J" first="Johanna A" last="Joyce">Johanna A. Joyce</name>
<affiliation><nlm:affiliation>1] Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA [2] Brain Tumor Center, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA [3] Metastasis Research Center, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.</nlm:affiliation>
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<series><title level="j">Nature cell biology</title>
<idno type="eISSN">1476-4679</idno>
<imprint><date when="2014" type="published">2014</date>
</imprint>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Antineoplastic Agents (pharmacology)</term>
<term>Biomarkers, Tumor (metabolism)</term>
<term>Blood-Brain Barrier (pathology)</term>
<term>Bone Neoplasms (enzymology)</term>
<term>Bone Neoplasms (mortality)</term>
<term>Bone Neoplasms (secondary)</term>
<term>Brain Neoplasms (enzymology)</term>
<term>Brain Neoplasms (mortality)</term>
<term>Brain Neoplasms (secondary)</term>
<term>Breast Neoplasms (enzymology)</term>
<term>Breast Neoplasms (mortality)</term>
<term>Breast Neoplasms (pathology)</term>
<term>Cathepsins (antagonists & inhibitors)</term>
<term>Cathepsins (physiology)</term>
<term>Cell Line, Tumor (MeSH)</term>
<term>Cell Movement (MeSH)</term>
<term>Cystatins (metabolism)</term>
<term>Disease-Free Survival (MeSH)</term>
<term>Female (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Kaplan-Meier Estimate (MeSH)</term>
<term>Lung Neoplasms (enzymology)</term>
<term>Lung Neoplasms (mortality)</term>
<term>Lung Neoplasms (secondary)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred NOD (MeSH)</term>
<term>Mice, Knockout (MeSH)</term>
<term>Mice, Nude (MeSH)</term>
<term>Mice, SCID (MeSH)</term>
<term>Organ Specificity (MeSH)</term>
<term>Protease Inhibitors (pharmacology)</term>
<term>Proteolysis (MeSH)</term>
<term>Serpins (metabolism)</term>
<term>Tight Junction Proteins (metabolism)</term>
<term>Tumor Microenvironment (MeSH)</term>
<term>Xenograft Model Antitumor Assays (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Cathepsins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Biomarkers, Tumor</term>
<term>Cystatins</term>
<term>Serpins</term>
<term>Tight Junction Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents</term>
<term>Protease Inhibitors</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Bone Neoplasms</term>
<term>Brain Neoplasms</term>
<term>Breast Neoplasms</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="mortality" xml:lang="en"><term>Bone Neoplasms</term>
<term>Brain Neoplasms</term>
<term>Breast Neoplasms</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Blood-Brain Barrier</term>
<term>Breast Neoplasms</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Cathepsins</term>
</keywords>
<keywords scheme="MESH" qualifier="secondary" xml:lang="en"><term>Bone Neoplasms</term>
<term>Brain Neoplasms</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Line, Tumor</term>
<term>Cell Movement</term>
<term>Disease-Free Survival</term>
<term>Female</term>
<term>Humans</term>
<term>Kaplan-Meier Estimate</term>
<term>Mice</term>
<term>Mice, Inbred NOD</term>
<term>Mice, Knockout</term>
<term>Mice, Nude</term>
<term>Mice, SCID</term>
<term>Organ Specificity</term>
<term>Proteolysis</term>
<term>Tumor Microenvironment</term>
<term>Xenograft Model Antitumor Assays</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Metastasis remains the most common cause of death in most cancers, with limited therapies for combating disseminated disease. While the primary tumour microenvironment is an important regulator of cancer progression, it is less well understood how different tissue environments influence metastasis. We analysed tumour-stroma interactions that modulate organ tropism of brain, bone and lung metastasis in xenograft models. We identified a number of potential modulators of site-specific metastasis, including cathepsin S as a regulator of breast-to-brain metastasis. High cathepsin S expression at the primary site correlated with decreased brain metastasis-free survival in breast cancer patients. Both macrophages and tumour cells produce cathepsin S, and only the combined depletion significantly reduced brain metastasis in vivo. Cathepsin S specifically mediates blood-brain barrier transmigration through proteolytic processing of the junctional adhesion molecule, JAM-B. Pharmacological inhibition of cathepsin S significantly reduced experimental brain metastasis, supporting its consideration as a therapeutic target for this disease.</div>
</front>
</TEI>
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<DateCompleted><Year>2014</Year>
<Month>10</Month>
<Day>28</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
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<JournalIssue CitedMedium="Internet"><Volume>16</Volume>
<Issue>9</Issue>
<PubDate><Year>2014</Year>
<Month>Sep</Month>
</PubDate>
</JournalIssue>
<Title>Nature cell biology</Title>
<ISOAbbreviation>Nat Cell Biol</ISOAbbreviation>
</Journal>
<ArticleTitle>Analysis of tumour- and stroma-supplied proteolytic networks reveals a brain-metastasis-promoting role for cathepsin S.</ArticleTitle>
<Pagination><MedlinePgn>876-88</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1038/ncb3011</ELocationID>
<Abstract><AbstractText>Metastasis remains the most common cause of death in most cancers, with limited therapies for combating disseminated disease. While the primary tumour microenvironment is an important regulator of cancer progression, it is less well understood how different tissue environments influence metastasis. We analysed tumour-stroma interactions that modulate organ tropism of brain, bone and lung metastasis in xenograft models. We identified a number of potential modulators of site-specific metastasis, including cathepsin S as a regulator of breast-to-brain metastasis. High cathepsin S expression at the primary site correlated with decreased brain metastasis-free survival in breast cancer patients. Both macrophages and tumour cells produce cathepsin S, and only the combined depletion significantly reduced brain metastasis in vivo. Cathepsin S specifically mediates blood-brain barrier transmigration through proteolytic processing of the junctional adhesion molecule, JAM-B. Pharmacological inhibition of cathepsin S significantly reduced experimental brain metastasis, supporting its consideration as a therapeutic target for this disease.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sevenich</LastName>
<ForeName>Lisa</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bowman</LastName>
<ForeName>Robert L</ForeName>
<Initials>RL</Initials>
<AffiliationInfo><Affiliation>1] Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA [2].</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Mason</LastName>
<ForeName>Steven D</ForeName>
<Initials>SD</Initials>
<AffiliationInfo><Affiliation>1] Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA [2].</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Quail</LastName>
<ForeName>Daniela F</ForeName>
<Initials>DF</Initials>
<AffiliationInfo><Affiliation>Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.</Affiliation>
</AffiliationInfo>
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<ForeName>Franck</ForeName>
<Initials>F</Initials>
<AffiliationInfo><Affiliation>Computational Biology Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Elie</LastName>
<ForeName>Benelita T</ForeName>
<Initials>BT</Initials>
<AffiliationInfo><Affiliation>Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Brogi</LastName>
<ForeName>Edi</ForeName>
<Initials>E</Initials>
<AffiliationInfo><Affiliation>Pathology Department, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Brastianos</LastName>
<ForeName>Priscilla K</ForeName>
<Initials>PK</Initials>
<AffiliationInfo><Affiliation>1] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [2] Division of Hematology/Oncology, Massachusetts General Hospital, Boston, Massachusetts 02214, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hahn</LastName>
<ForeName>William C</ForeName>
<Initials>WC</Initials>
<AffiliationInfo><Affiliation>Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Holsinger</LastName>
<ForeName>Leslie J</ForeName>
<Initials>LJ</Initials>
<AffiliationInfo><Affiliation>Virobay Inc., 1360 Willow Road, Menlo Park, California 94025, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Massagué</LastName>
<ForeName>Joan</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>1] Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA [2] Brain Tumor Center, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA [3] Metastasis Research Center, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Leslie</LastName>
<ForeName>Christina S</ForeName>
<Initials>CS</Initials>
<AffiliationInfo><Affiliation>Computational Biology Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Joyce</LastName>
<ForeName>Johanna A</ForeName>
<Initials>JA</Initials>
<AffiliationInfo><Affiliation>1] Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA [2] Brain Tumor Center, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA [3] Metastasis Research Center, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>F32 CA130329</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>CA126518</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>CA148967</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>F31 CA167863</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>P01 CA142536</GrantID>
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Analysis of tumour- and stroma-supplied proteolytic networks reveals a brain-metastasis-promoting role for cathepsin S.

Analysis of tumour- and stroma-supplied proteolytic networks reveals a brain-metastasis-promoting role for cathepsin S.

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