Lysosomes and unfolded protein response, determinants of differential resistance of melanoma cells to vinca alkaloids
Identifieur interne : 000804 ( Istex/Corpus ); précédent : 000803; suivant : 000805Lysosomes and unfolded protein response, determinants of differential resistance of melanoma cells to vinca alkaloids
Auteurs : Laure-Anais Vincent ; Chaker Attaoua ; Michel Bellis ; Lucie Rozkydalova ; Kamel Hadj-Kaddour ; Laurence Vian ; Pierre CuqSource :
- Fundamental & Clinical Pharmacology [ 0767-3981 ] ; 2015-04.
Abstract
On account of its strong ability to become chemoresistant after a primary response to drugs, malignant melanoma (MM) remains a therapeutic challenge. This study focuses on acquired resistance to vinca alkaloids (VAs) using VA‐resistant MM cell lines (CAL1R‐VCR, CAL1R‐VDS, and CAL1R‐VRB), established by long‐term continuous exposure of parental CAL1‐wt cells to vincristine (VCR), vindesine (VDS), or vinorelbine (VRB), respectively. Transcriptomic profiling using rma and rdam methods led to distinguish two cell groups: CAL1R‐VCR and CAL1R‐VDS, CAL1R‐VRB, and CAL1‐wt. mgsa of the specifically altered genes in the first group evidenced the GO terms ‘lysosomal lumen’ and ‘vacuolar lumen’ linked to underexpressed genes, and ‘endoplasmic reticulum (ER) stress response’ associated with overexpressed genes. A specific reduction of lysosomal enzymes, independent of acidic vacuole organelle (AVO) turnover, was observed (LTG probe) in CAL1R‐VCR and CAL1R‐VDS cells. It was associated with the specific lowering of cathepsin B and L, known to be involved in the lysosomal pathway of apoptosis. Confirming gene profiling, the same groups (CAL1R‐VCR and CAL1R‐VDS, CAL1‐wt and CAL1R‐VRB) could be distinguished regarding the VA‐mediated changes on mean size areas and on acidic compartment volumes. These two parameters were reduced in CAL1R‐VCR and CAL1R‐VDS cells, suggesting a smaller AVO accumulation and thus a reduced sensitivity to lysosomal membrane permeabilization‐mediated apoptosis. In addition, ‘ER stress response’ inhibition by tauroursodeoxycholic acid induced a higher VA sensitization of the first cell group. In conclusion, lysosomes and unfolded protein response could be key determinants of the differential resistance of MM to VAs.
Url:
DOI: 10.1111/fcp.12098
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ISTEX:77B006757A459C9E70C35165922D5B5A52AAF069Le document en format XML
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last="Attaoua">Chaker Attaoua</name><affiliation><mods:affiliation>Laboratoire de Toxicologie du Médicament, Institut des Biomolécules Max Mousseron (UMR5247), UFR des Sciences Pharmaceutiques et Biologiques, Université de Montpellier, 15 Avenue Charles Flahault, BP14491, 34093, Montpellier Cedex 05, France</mods:affiliation></affiliation></author><author><name sortKey="Bellis, Michel" sort="Bellis, Michel" uniqKey="Bellis M" first="Michel" last="Bellis">Michel Bellis</name><affiliation><mods:affiliation>Centre de Recherche de Biochimie Macromoléculaire (CRBM), UMR 5237, CNRS, 1919 Route de Mende, 34293, Montpellier Cedex, France</mods:affiliation></affiliation></author><author><name sortKey="Rozkydalova, Lucie" sort="Rozkydalova, Lucie" uniqKey="Rozkydalova L" first="Lucie" last="Rozkydalova">Lucie Rozkydalova</name><affiliation><mods:affiliation>Laboratoire de Toxicologie du Médicament, Institut des Biomolécules Max Mousseron (UMR5247), UFR des Sciences Pharmaceutiques et Biologiques, Université de Montpellier, 15 Avenue Charles Flahault, BP14491, 34093, Montpellier Cedex 05, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Pharmacology and Toxicology, Faculty of Pharmacy in Hradec Kralove, Charles University in Prague, Heyrovskeho 1203, 500 05, Hradec Kralove, Czech Republic</mods:affiliation></affiliation></author><author><name sortKey="Hadj Addour, Kamel" sort="Hadj Addour, Kamel" uniqKey="Hadj Addour K" first="Kamel" last="Hadj-Kaddour">Kamel Hadj-Kaddour</name><affiliation><mods:affiliation>Laboratoire de Toxicologie du Médicament, Institut des Biomolécules Max Mousseron (UMR5247), UFR des Sciences Pharmaceutiques et Biologiques, Université de Montpellier, 15 Avenue Charles Flahault, BP14491, 34093, Montpellier Cedex 05, France</mods:affiliation></affiliation></author><author><name sortKey="Vian, Laurence" sort="Vian, Laurence" uniqKey="Vian L" first="Laurence" last="Vian">Laurence Vian</name><affiliation><mods:affiliation>Laboratoire de Toxicologie du Médicament, Institut des Biomolécules Max Mousseron (UMR5247), UFR des Sciences Pharmaceutiques et Biologiques, Université de Montpellier, 15 Avenue Charles Flahault, BP14491, 34093, Montpellier Cedex 05, France</mods:affiliation></affiliation></author><author><name sortKey="Cuq, Pierre" sort="Cuq, Pierre" uniqKey="Cuq P" first="Pierre" last="Cuq">Pierre Cuq</name><affiliation><mods:affiliation>Laboratoire de Toxicologie du Médicament, Institut des Biomolécules Max Mousseron (UMR5247), UFR des Sciences Pharmaceutiques et Biologiques, Université de Montpellier, 15 Avenue Charles Flahault, BP14491, 34093, Montpellier Cedex 05, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Correspondence and reprints:</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: pierre.cuq@univ-montp1.fr</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Fundamental & Clinical Pharmacology</title><title level="j" type="alt">FUNDAMENTAL AND CLINICAL PHARMACOLOGY</title><idno type="ISSN">0767-3981</idno><idno type="eISSN">1472-8206</idno><imprint><biblScope unit="vol">29</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="164">164</biblScope><biblScope unit="page" to="177">177</biblScope><biblScope unit="page-count">14</biblScope><date type="published" when="2015-04">2015-04</date></imprint><idno type="ISSN">0767-3981</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0767-3981</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">On account of its strong ability to become chemoresistant after a primary response to drugs, malignant melanoma (MM) remains a therapeutic challenge. This study focuses on acquired resistance to vinca alkaloids (VAs) using VA‐resistant MM cell lines (CAL1R‐VCR, CAL1R‐VDS, and CAL1R‐VRB), established by long‐term continuous exposure of parental CAL1‐wt cells to vincristine (VCR), vindesine (VDS), or vinorelbine (VRB), respectively. Transcriptomic profiling using rma and rdam methods led to distinguish two cell groups: CAL1R‐VCR and CAL1R‐VDS, CAL1R‐VRB, and CAL1‐wt. mgsa of the specifically altered genes in the first group evidenced the GO terms ‘lysosomal lumen’ and ‘vacuolar lumen’ linked to underexpressed genes, and ‘endoplasmic reticulum (ER) stress response’ associated with overexpressed genes. A specific reduction of lysosomal enzymes, independent of acidic vacuole organelle (AVO) turnover, was observed (LTG probe) in CAL1R‐VCR and CAL1R‐VDS cells. It was associated with the specific lowering of cathepsin B and L, known to be involved in the lysosomal pathway of apoptosis. Confirming gene profiling, the same groups (CAL1R‐VCR and CAL1R‐VDS, CAL1‐wt and CAL1R‐VRB) could be distinguished regarding the VA‐mediated changes on mean size areas and on acidic compartment volumes. These two parameters were reduced in CAL1R‐VCR and CAL1R‐VDS cells, suggesting a smaller AVO accumulation and thus a reduced sensitivity to lysosomal membrane permeabilization‐mediated apoptosis. In addition, ‘ER stress response’ inhibition by tauroursodeoxycholic acid induced a higher VA sensitization of the first cell group. 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Cedex 05, France</json:string></affiliations></json:item><json:item><name>Michel Bellis</name><affiliations><json:string>Centre de Recherche de Biochimie Macromoléculaire (CRBM), UMR 5237, CNRS, 1919 Route de Mende, 34293, Montpellier Cedex, France</json:string></affiliations></json:item><json:item><name>Lucie Rozkydalova</name><affiliations><json:string>Laboratoire de Toxicologie du Médicament, Institut des Biomolécules Max Mousseron (UMR5247), UFR des Sciences Pharmaceutiques et Biologiques, Université de Montpellier, 15 Avenue Charles Flahault, BP14491, 34093, Montpellier Cedex 05, France</json:string><json:string>Department of Pharmacology and Toxicology, Faculty of Pharmacy in Hradec Kralove, Charles University in Prague, Heyrovskeho 1203, 500 05, Hradec Kralove, Czech Republic</json:string></affiliations></json:item><json:item><name>Kamel Hadj‐Kaddour</name><affiliations><json:string>Laboratoire de Toxicologie du Médicament, Institut des Biomolécules Max Mousseron (UMR5247), UFR des Sciences Pharmaceutiques et Biologiques, Université de Montpellier, 15 Avenue Charles Flahault, BP14491, 34093, Montpellier Cedex 05, France</json:string></affiliations></json:item><json:item><name>Laurence Vian</name><affiliations><json:string>Laboratoire de Toxicologie du Médicament, Institut des Biomolécules Max Mousseron (UMR5247), UFR des Sciences Pharmaceutiques et Biologiques, Université de Montpellier, 15 Avenue Charles Flahault, BP14491, 34093, Montpellier Cedex 05, France</json:string></affiliations></json:item><json:item><name>Pierre Cuq</name><affiliations><json:string>Laboratoire de Toxicologie du Médicament, Institut des Biomolécules Max Mousseron (UMR5247), UFR des Sciences Pharmaceutiques et Biologiques, Université de Montpellier, 15 Avenue Charles Flahault, BP14491, 34093, Montpellier Cedex 05, France</json:string><json:string>Correspondence and reprints:</json:string><json:string>E-mail: pierre.cuq@univ-montp1.fr</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>lysosomes</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>melanoma</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>microarray analysis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neoplasm drug resistance</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>unfolded protein response</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>vinca alkaloids</value></json:item></subject><articleId><json:string>FCP12098</json:string></articleId><arkIstex>ark:/67375/WNG-6QP0CWZN-W</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>On account of its strong ability to become chemoresistant after a primary response to drugs, malignant melanoma (MM) remains a therapeutic challenge. This study focuses on acquired resistance to vinca alkaloids (VAs) using VA‐resistant MM cell lines (CAL1R‐VCR, CAL1R‐VDS, and CAL1R‐VRB), established by long‐term continuous exposure of parental CAL1‐wt cells to vincristine (VCR), vindesine (VDS), or vinorelbine (VRB), respectively. Transcriptomic profiling using rma and rdam methods led to distinguish two cell groups: CAL1R‐VCR and CAL1R‐VDS, CAL1R‐VRB, and CAL1‐wt. mgsa of the specifically altered genes in the first group evidenced the GO terms ‘lysosomal lumen’ and ‘vacuolar lumen’ linked to underexpressed genes, and ‘endoplasmic reticulum (ER) stress response’ associated with overexpressed genes. A specific reduction of lysosomal enzymes, independent of acidic vacuole organelle (AVO) turnover, was observed (LTG probe) in CAL1R‐VCR and CAL1R‐VDS cells. It was associated with the specific lowering of cathepsin B and L, known to be involved in the lysosomal pathway of apoptosis. Confirming gene profiling, the same groups (CAL1R‐VCR and CAL1R‐VDS, CAL1‐wt and CAL1R‐VRB) could be distinguished regarding the VA‐mediated changes on mean size areas and on acidic compartment volumes. These two parameters were reduced in CAL1R‐VCR and CAL1R‐VDS cells, suggesting a smaller AVO accumulation and thus a reduced sensitivity to lysosomal membrane permeabilization‐mediated apoptosis. In addition, ‘ER stress response’ inhibition by tauroursodeoxycholic acid induced a higher VA sensitization of the first cell group. 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<orgName type="division">Institut des Biomolécules Max Mousseron (UMR5247)</orgName>
<orgName type="division">UFR des Sciences Pharmaceutiques et Biologiques</orgName>
<orgName type="institution">Université de Montpellier</orgName>
<address><street>15 Avenue Charles Flahault, BP14491</street>
<postCode>34093</postCode>
<settlement>Montpellier Cedex 05</settlement>
<country key="FR" xml:lang="en">FRANCE</country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Michel</forename><surname>Bellis</surname></persName><affiliation><orgName type="division">Centre de Recherche de Biochimie Macromoléculaire (CRBM)</orgName>
<orgName type="division">UMR 5237</orgName>
<orgName type="institution">CNRS</orgName>
<address><street>1919 Route de Mende</street>
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<country key="FR" xml:lang="en">FRANCE</country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Lucie</forename><surname>Rozkydalova</surname></persName><affiliation><orgName type="division">Laboratoire de Toxicologie du Médicament</orgName>
<orgName type="division">Institut des Biomolécules Max Mousseron (UMR5247)</orgName>
<orgName type="division">UFR des Sciences Pharmaceutiques et Biologiques</orgName>
<orgName type="institution">Université de Montpellier</orgName>
<address><street>15 Avenue Charles Flahault, BP14491</street>
<postCode>34093</postCode>
<settlement>Montpellier Cedex 05</settlement>
<country key="FR" xml:lang="en">FRANCE</country></address></affiliation><affiliation><orgName type="division">Department of Pharmacology and Toxicology</orgName>
<orgName type="division">Faculty of Pharmacy in Hradec Kralove</orgName>
<orgName type="institution">Charles University in Prague</orgName>
<address><street>Heyrovskeho 1203</street>
<postCode>500 05</postCode>
<settlement>Hradec Kralove</settlement>
<country key="CZ" xml:lang="en">CZECH REPUBLIC</country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Kamel</forename><surname>Hadj‐Kaddour</surname></persName><affiliation><orgName type="division">Laboratoire de Toxicologie du Médicament</orgName>
<orgName type="division">Institut des Biomolécules Max Mousseron (UMR5247)</orgName>
<orgName type="division">UFR des Sciences Pharmaceutiques et Biologiques</orgName>
<orgName type="institution">Université de Montpellier</orgName>
<address><street>15 Avenue Charles Flahault, BP14491</street>
<postCode>34093</postCode>
<settlement>Montpellier Cedex 05</settlement>
<country key="FR" xml:lang="en">FRANCE</country></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">Laurence</forename><surname>Vian</surname></persName><affiliation><orgName type="division">Laboratoire de Toxicologie du Médicament</orgName>
<orgName type="division">Institut des Biomolécules Max Mousseron (UMR5247)</orgName>
<orgName type="division">UFR des Sciences Pharmaceutiques et Biologiques</orgName>
<orgName type="institution">Université de Montpellier</orgName>
<address><street>15 Avenue Charles Flahault, BP14491</street>
<postCode>34093</postCode>
<settlement>Montpellier Cedex 05</settlement>
<country key="FR" xml:lang="en">FRANCE</country></address></affiliation></author><author xml:id="author-0006" role="corresp"><persName><forename type="first">Pierre</forename><surname>Cuq</surname></persName><affiliation><orgName type="division">Laboratoire de Toxicologie du Médicament</orgName>
<orgName type="division">Institut des Biomolécules Max Mousseron (UMR5247)</orgName>
<orgName type="division">UFR des Sciences Pharmaceutiques et Biologiques</orgName>
<orgName type="institution">Université de Montpellier</orgName>
<address><street>15 Avenue Charles Flahault, BP14491</street>
<postCode>34093</postCode>
<settlement>Montpellier Cedex 05</settlement>
<country key="FR" xml:lang="en">FRANCE</country></address></affiliation></author><idno type="istex">77B006757A459C9E70C35165922D5B5A52AAF069</idno><idno type="ark">ark:/67375/WNG-6QP0CWZN-W</idno><idno type="DOI">10.1111/fcp.12098</idno><idno type="unit">FCP12098</idno><idno type="toTypesetVersion">file:FCP.FCP12098.pdf</idno></analytic><monogr><title level="j" type="main">Fundamental & Clinical Pharmacology</title><title level="j" type="alt">FUNDAMENTAL AND CLINICAL PHARMACOLOGY</title><idno type="pISSN">0767-3981</idno><idno type="eISSN">1472-8206</idno><idno type="book-DOI">10.1111/(ISSN)1472-8206</idno><idno type="book-part-DOI">10.1111/fcp.2015.29.issue-2</idno><idno type="product">FCP</idno><imprint><biblScope unit="vol">29</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="164">164</biblScope><biblScope unit="page" to="177">177</biblScope><biblScope unit="page-count">14</biblScope><date type="published" when="2015-04"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><encodingDesc><schemaRef type="ODD" url="https://xml-schema.delivery.istex.fr/tei-istex.odd"></schemaRef><appInfo><application ident="pub2tei" version="1.0.10" when="2019-12-20"><label>pub2TEI-ISTEX</label><desc>A set of style sheets for converting XML documents encoded in various scientific publisher formats into a common TEI format.
<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract style="main" xml:id="fcp12098-abs-0001"><head>Abstract</head><p>On account of its strong ability to become chemoresistant after a primary response to drugs, malignant melanoma (<hi rend="fc">MM</hi>) remains a therapeutic challenge. This study focuses on acquired resistance to vinca alkaloids (<hi rend="fc">VA</hi>s) using <hi rend="fc">VA</hi>‐resistant <hi rend="fc">MM</hi> cell lines (<hi rend="fc">CAL</hi>1<hi rend="fc">R</hi>‐<hi rend="fc">VCR</hi>,<hi rend="fc"> CAL</hi>1<hi rend="fc">R</hi>‐<hi rend="fc">VDS</hi>, and <hi rend="fc">CAL</hi>1<hi rend="fc">R</hi>‐<hi rend="fc">VRB</hi>), established by long‐term continuous exposure of parental <hi rend="fc">CAL</hi>1‐wt cells to vincristine (<hi rend="fc">VCR</hi>), vindesine (<hi rend="fc">VDS</hi>), or vinorelbine (<hi rend="fc">VRB</hi>), respectively. Transcriptomic profiling using <hi rend="smallCaps">rma</hi> and <hi rend="smallCaps">rdam</hi> methods led to distinguish two cell groups: <hi rend="fc">CAL</hi>1<hi rend="fc">R</hi>‐<hi rend="fc">VCR</hi> and <hi rend="fc">CAL</hi>1R‐<hi rend="fc">VDS</hi>,<hi rend="fc"> CAL</hi>1<hi rend="fc">R</hi>‐<hi rend="fc">VRB</hi>, and <hi rend="fc">CAL</hi>1‐wt. <hi rend="smallCaps">mgsa</hi> of the specifically altered genes in the first group evidenced the <hi rend="fc">GO</hi> terms ‘lysosomal lumen’ and ‘vacuolar lumen’ linked to underexpressed genes, and ‘endoplasmic reticulum (<hi rend="fc">ER</hi>) stress response’ associated with overexpressed genes. A specific reduction of lysosomal enzymes, independent of acidic vacuole organelle (<hi rend="fc">AVO</hi>) turnover, was observed (<hi rend="fc">LTG</hi> probe) in <hi rend="fc">CAL</hi>1<hi rend="fc">R</hi>‐<hi rend="fc">VCR</hi> and <hi rend="fc">CAL</hi>1<hi rend="fc">R</hi>‐<hi rend="fc">VDS</hi> cells. It was associated with the specific lowering of cathepsin <hi rend="fc">B</hi> and <hi rend="fc">L</hi>, known to be involved in the lysosomal pathway of apoptosis. Confirming gene profiling, the same groups (<hi rend="fc">CAL</hi>1<hi rend="fc">R</hi>‐<hi rend="fc">VCR</hi> and <hi rend="fc">CAL</hi>1<hi rend="fc">R</hi>‐<hi rend="fc">VDS</hi>,<hi rend="fc"> CAL</hi>1‐wt and <hi rend="fc">CAL</hi>1<hi rend="fc">R</hi>‐<hi rend="fc">VRB</hi>) could be distinguished regarding the <hi rend="fc">VA</hi>‐mediated changes on mean size areas and on acidic compartment volumes. These two parameters were reduced in <hi rend="fc">CAL</hi>1<hi rend="fc">R</hi>‐<hi rend="fc">VCR</hi> and <hi rend="fc">CAL</hi>1<hi rend="fc">R</hi>‐<hi rend="fc">VDS</hi> cells, suggesting a smaller <hi rend="fc">AVO</hi> accumulation and thus a reduced sensitivity to lysosomal membrane permeabilization‐mediated apoptosis. In addition, ‘<hi rend="fc">ER</hi> stress response’ inhibition by tauroursodeoxycholic acid induced a higher <hi rend="fc">VA</hi> sensitization of the first cell group. In conclusion, lysosomes and unfolded protein response could be key determinants of the differential resistance of <hi rend="fc">MM</hi> to <hi rend="fc">VA</hi>s.</p></abstract><textClass><keywords><term xml:id="fcp12098-kwd-0001">lysosomes</term><term xml:id="fcp12098-kwd-0002">melanoma</term><term xml:id="fcp12098-kwd-0003">microarray analysis</term><term xml:id="fcp12098-kwd-0004">neoplasm drug resistance</term><term xml:id="fcp12098-kwd-0005">unfolded protein response</term><term xml:id="fcp12098-kwd-0006">vinca alkaloids</term></keywords><keywords rend="articleCategory"><term>Original Article</term></keywords><keywords rend="tocHeading1"><term>ORIGINAL ARTICLES</term></keywords><keywords rend="tocHeading2"><term>FUNDAMENTAL PHARMACOLOGY</term></keywords><keywords rend="tocHeading3"><term>Oncopharmacology</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-6QP0CWZN-W/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component type="serialArticle" version="2.0" xml:id="fcp12098" xml:lang="en"><header><publicationMeta level="product"><doi origin="wiley" registered="yes">10.1111/(ISSN)1472-8206</doi><issn type="print">0767-3981</issn><issn type="electronic">1472-8206</issn><idGroup><id type="product" value="FCP"></id></idGroup><titleGroup><title sort="FUNDAMENTAL AND CLINICAL PHARMACOLOGY" type="main">Fundamental & Clinical Pharmacology</title><title type="short">Fundam Clin Pharmacol</title></titleGroup></publicationMeta><publicationMeta level="part" position="20"><doi origin="wiley">10.1111/fcp.2015.29.issue-2</doi><copyright ownership="thirdParty">Copyright © 2015 Société Française de Pharmacologie et de Thérapeutique</copyright><numberingGroup><numbering type="journalVolume" number="29">29</numbering><numbering type="journalIssue">2</numbering></numberingGroup><coverDate startDate="2015-04">April 2015</coverDate></publicationMeta><publicationMeta level="unit" position="40" status="forIssue" type="article"><doi>10.1111/fcp.12098</doi><idGroup><id type="unit" value="FCP12098"></id></idGroup><countGroup><count number="14" type="pageTotal"></count></countGroup><titleGroup><title type="articleCategory">Original Article</title><title type="tocHeading1">ORIGINAL ARTICLES</title><title type="tocHeading2">FUNDAMENTAL PHARMACOLOGY</title><title type="tocHeading3">Oncopharmacology</title></titleGroup><copyright ownership="thirdParty">© 2015 Société Française de Pharmacologie et de Thérapeutique</copyright><eventGroup><event date="2014-10-13" type="manuscriptReceived"></event><event date="2014-12-18" type="manuscriptRevised"></event><event date="2014-12-24" type="manuscriptAccepted"></event><event agent="SPS" date="2015-01-17" type="xmlCreated"></event><event type="publishedOnlineAccepted" date="2015-01-20"></event><event type="publishedOnlineEarlyUnpaginated" date="2015-02-27"></event><event type="firstOnline" date="2015-02-27"></event><event type="publishedOnlineFinalForm" date="2015-03-16"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.7.2 mode:FullText" date="2016-01-05"></event></eventGroup><numberingGroup><numbering type="pageFirst">164</numbering><numbering type="pageLast">177</numbering></numberingGroup><correspondenceTo><lineatedText><line>Correspondence and reprints:</line><line><email>pierre.cuq@univ-montp1.fr</email></line></lineatedText></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:FCP.FCP12098.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main">Lysosomes and unfolded protein response, determinants of differential resistance of melanoma cells to vinca alkaloids</title><title type="shortAuthors">L.‐A. Vincent <i>et al</i>.</title></titleGroup><creators><creator affiliationRef="#fcp12098-aff-0001" creatorRole="author" xml:id="fcp12098-cr-0001"><personName><givenNames>Laure‐Anais</givenNames> <familyName>Vincent</familyName></personName></creator><creator affiliationRef="#fcp12098-aff-0001" creatorRole="author" xml:id="fcp12098-cr-0002"><personName><givenNames>Chaker</givenNames> <familyName>Attaoua</familyName></personName></creator><creator affiliationRef="#fcp12098-aff-0002" creatorRole="author" xml:id="fcp12098-cr-0003"><personName><givenNames>Michel</givenNames> <familyName>Bellis</familyName></personName></creator><creator affiliationRef="#fcp12098-aff-0001 #fcp12098-aff-0003" creatorRole="author" xml:id="fcp12098-cr-0004"><personName><givenNames>Lucie</givenNames> <familyName>Rozkydalova</familyName></personName></creator><creator affiliationRef="#fcp12098-aff-0001" creatorRole="author" xml:id="fcp12098-cr-0005"><personName><givenNames>Kamel</givenNames> <familyName>Hadj‐Kaddour</familyName></personName></creator><creator affiliationRef="#fcp12098-aff-0001" creatorRole="author" xml:id="fcp12098-cr-0006"><personName><givenNames>Laurence</givenNames> <familyName>Vian</familyName></personName></creator><creator affiliationRef="#fcp12098-aff-0001" corresponding="yes" creatorRole="author" xml:id="fcp12098-cr-0007"><personName><givenNames>Pierre</givenNames> <familyName>Cuq</familyName></personName></creator></creators><affiliationGroup><affiliation countryCode="FR" type="organization" xml:id="fcp12098-aff-0001"><orgDiv>Laboratoire de Toxicologie du Médicament</orgDiv> <orgDiv>Institut des Biomolécules Max Mousseron (UMR5247)</orgDiv> <orgDiv>UFR des Sciences Pharmaceutiques et Biologiques</orgDiv> <orgName>Université de Montpellier</orgName> <address><street>15 Avenue Charles Flahault, BP14491</street> <postCode>34093</postCode> <city>Montpellier Cedex 05</city> <country>France</country></address></affiliation><affiliation countryCode="FR" type="organization" xml:id="fcp12098-aff-0002"><orgDiv>Centre de Recherche de Biochimie Macromoléculaire (CRBM)</orgDiv> <orgDiv>UMR 5237</orgDiv> <orgName>CNRS</orgName> <address><street>1919 Route de Mende</street> <postCode>34293</postCode> <city>Montpellier Cedex</city> <country>France</country></address></affiliation><affiliation countryCode="CZ" type="organization" xml:id="fcp12098-aff-0003"><orgDiv>Department of Pharmacology and Toxicology</orgDiv> <orgDiv>Faculty of Pharmacy in Hradec Kralove</orgDiv> <orgName>Charles University in Prague</orgName> <address><street>Heyrovskeho 1203</street> <postCode>500 05</postCode> <city>Hradec Kralove</city> <country>Czech Republic</country></address></affiliation></affiliationGroup><keywordGroup type="author"><keyword xml:id="fcp12098-kwd-0001">lysosomes</keyword><keyword xml:id="fcp12098-kwd-0002">melanoma</keyword><keyword xml:id="fcp12098-kwd-0003">microarray analysis</keyword><keyword xml:id="fcp12098-kwd-0004">neoplasm drug resistance</keyword><keyword xml:id="fcp12098-kwd-0005">unfolded protein response</keyword><keyword xml:id="fcp12098-kwd-0006">vinca alkaloids</keyword></keywordGroup><fundingInfo><fundingAgency>GEFLUC‐LR</fundingAgency><fundingNumber>DC/MLP/09‐011</fundingNumber></fundingInfo><fundingInfo><fundingAgency>GENCI‐CINES</fundingAgency><fundingNumber>c2014035038</fundingNumber></fundingInfo><supportingInformation><supportingInfoItem><mediaResource alt="supporting" mimeType="application/msword" href="urn-x:wiley:07673981:media:fcp12098:fcp12098-sup-0001-TableS1"></mediaResource><caption><b>Table S1.</b> Complementary data of GO term enrichment analysis of genes up‐ and down‐regulated in <fc>VA</fc> resistant cells using <sc>ontologizer</sc> software.</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:id="fcp12098-abs-0001"><title type="main">Abstract</title><p>On account of its strong ability to become chemoresistant after a primary response to drugs, malignant melanoma (<fc>MM</fc>) remains a therapeutic challenge. This study focuses on acquired resistance to vinca alkaloids (<fc>VA</fc>s) using <fc>VA</fc>‐resistant <fc>MM</fc> cell lines (<fc>CAL</fc>1<fc>R</fc>‐<fc>VCR</fc>,<fc> CAL</fc>1<fc>R</fc>‐<fc>VDS</fc>, and <fc>CAL</fc>1<fc>R</fc>‐<fc>VRB</fc>), established by long‐term continuous exposure of parental <fc>CAL</fc>1‐wt cells to vincristine (<fc>VCR</fc>), vindesine (<fc>VDS</fc>), or vinorelbine (<fc>VRB</fc>), respectively. Transcriptomic profiling using <sc>rma</sc> and <sc>rdam</sc> methods led to distinguish two cell groups: <fc>CAL</fc>1<fc>R</fc>‐<fc>VCR</fc> and <fc>CAL</fc>1R‐<fc>VDS</fc>,<fc> CAL</fc>1<fc>R</fc>‐<fc>VRB</fc>, and <fc>CAL</fc>1‐wt. <sc>mgsa</sc> of the specifically altered genes in the first group evidenced the <fc>GO</fc> terms ‘lysosomal lumen’ and ‘vacuolar lumen’ linked to underexpressed genes, and ‘endoplasmic reticulum (<fc>ER</fc>) stress response’ associated with overexpressed genes. A specific reduction of lysosomal enzymes, independent of acidic vacuole organelle (<fc>AVO</fc>) turnover, was observed (<fc>LTG</fc> probe) in <fc>CAL</fc>1<fc>R</fc>‐<fc>VCR</fc> and <fc>CAL</fc>1<fc>R</fc>‐<fc>VDS</fc> cells. It was associated with the specific lowering of cathepsin <fc>B</fc> and <fc>L</fc>, known to be involved in the lysosomal pathway of apoptosis. Confirming gene profiling, the same groups (<fc>CAL</fc>1<fc>R</fc>‐<fc>VCR</fc> and <fc>CAL</fc>1<fc>R</fc>‐<fc>VDS</fc>,<fc> CAL</fc>1‐wt and <fc>CAL</fc>1<fc>R</fc>‐<fc>VRB</fc>) could be distinguished regarding the <fc>VA</fc>‐mediated changes on mean size areas and on acidic compartment volumes. These two parameters were reduced in <fc>CAL</fc>1<fc>R</fc>‐<fc>VCR</fc> and <fc>CAL</fc>1<fc>R</fc>‐<fc>VDS</fc> cells, suggesting a smaller <fc>AVO</fc> accumulation and thus a reduced sensitivity to lysosomal membrane permeabilization‐mediated apoptosis. In addition, ‘<fc>ER</fc> stress response’ inhibition by tauroursodeoxycholic acid induced a higher <fc>VA</fc> sensitization of the first cell group. In conclusion, lysosomes and unfolded protein response could be key determinants of the differential resistance of <fc>MM</fc> to <fc>VA</fc>s.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Lysosomes and unfolded protein response, determinants of differential resistance of melanoma cells to vinca alkaloids</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Lysosomes and unfolded protein response, determinants of differential resistance of melanoma cells to vinca alkaloids</title></titleInfo><name type="personal"><namePart type="given">Laure‐Anais</namePart><namePart type="family">Vincent</namePart><affiliation>Laboratoire de Toxicologie du Médicament, Institut des Biomolécules Max Mousseron (UMR5247), UFR des Sciences Pharmaceutiques et Biologiques, Université de Montpellier, 15 Avenue Charles Flahault, BP14491, 34093, Montpellier Cedex 05, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Chaker</namePart><namePart type="family">Attaoua</namePart><affiliation>Laboratoire de Toxicologie du Médicament, Institut des Biomolécules Max Mousseron (UMR5247), UFR des Sciences Pharmaceutiques et Biologiques, Université de Montpellier, 15 Avenue Charles Flahault, BP14491, 34093, Montpellier Cedex 05, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michel</namePart><namePart type="family">Bellis</namePart><affiliation>Centre de Recherche de Biochimie Macromoléculaire (CRBM), UMR 5237, CNRS, 1919 Route de Mende, 34293, Montpellier Cedex, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Lucie</namePart><namePart type="family">Rozkydalova</namePart><affiliation>Laboratoire de Toxicologie du Médicament, Institut des Biomolécules Max Mousseron (UMR5247), UFR des Sciences Pharmaceutiques et Biologiques, Université de Montpellier, 15 Avenue Charles Flahault, BP14491, 34093, Montpellier Cedex 05, France</affiliation><affiliation>Department of Pharmacology and Toxicology, Faculty of Pharmacy in Hradec Kralove, Charles University in Prague, Heyrovskeho 1203, 500 05, Hradec Kralove, Czech Republic</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kamel</namePart><namePart type="family">Hadj‐Kaddour</namePart><affiliation>Laboratoire de Toxicologie du Médicament, Institut des Biomolécules Max Mousseron (UMR5247), UFR des Sciences Pharmaceutiques et Biologiques, Université de Montpellier, 15 Avenue Charles Flahault, BP14491, 34093, Montpellier Cedex 05, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Laurence</namePart><namePart type="family">Vian</namePart><affiliation>Laboratoire de Toxicologie du Médicament, Institut des Biomolécules Max Mousseron (UMR5247), UFR des Sciences Pharmaceutiques et Biologiques, Université de Montpellier, 15 Avenue Charles Flahault, BP14491, 34093, Montpellier Cedex 05, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Pierre</namePart><namePart type="family">Cuq</namePart><affiliation>Laboratoire de Toxicologie du Médicament, Institut des Biomolécules Max Mousseron (UMR5247), UFR des Sciences Pharmaceutiques et Biologiques, Université de Montpellier, 15 Avenue Charles Flahault, BP14491, 34093, Montpellier Cedex 05, France</affiliation><affiliation>Correspondence and reprints:</affiliation><affiliation>E-mail: pierre.cuq@univ-montp1.fr</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><dateIssued encoding="w3cdtf">2015-04</dateIssued><dateCreated encoding="w3cdtf">2015-01-17</dateCreated><dateCaptured encoding="w3cdtf">2014-10-13</dateCaptured><dateValid encoding="w3cdtf">2014-12-24</dateValid><copyrightDate encoding="w3cdtf">2015</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract>On account of its strong ability to become chemoresistant after a primary response to drugs, malignant melanoma (MM) remains a therapeutic challenge. This study focuses on acquired resistance to vinca alkaloids (VAs) using VA‐resistant MM cell lines (CAL1R‐VCR, CAL1R‐VDS, and CAL1R‐VRB), established by long‐term continuous exposure of parental CAL1‐wt cells to vincristine (VCR), vindesine (VDS), or vinorelbine (VRB), respectively. Transcriptomic profiling using rma and rdam methods led to distinguish two cell groups: CAL1R‐VCR and CAL1R‐VDS, CAL1R‐VRB, and CAL1‐wt. mgsa of the specifically altered genes in the first group evidenced the GO terms ‘lysosomal lumen’ and ‘vacuolar lumen’ linked to underexpressed genes, and ‘endoplasmic reticulum (ER) stress response’ associated with overexpressed genes. A specific reduction of lysosomal enzymes, independent of acidic vacuole organelle (AVO) turnover, was observed (LTG probe) in CAL1R‐VCR and CAL1R‐VDS cells. It was associated with the specific lowering of cathepsin B and L, known to be involved in the lysosomal pathway of apoptosis. Confirming gene profiling, the same groups (CAL1R‐VCR and CAL1R‐VDS, CAL1‐wt and CAL1R‐VRB) could be distinguished regarding the VA‐mediated changes on mean size areas and on acidic compartment volumes. These two parameters were reduced in CAL1R‐VCR and CAL1R‐VDS cells, suggesting a smaller AVO accumulation and thus a reduced sensitivity to lysosomal membrane permeabilization‐mediated apoptosis. In addition, ‘ER stress response’ inhibition by tauroursodeoxycholic acid induced a higher VA sensitization of the first cell group. In conclusion, lysosomes and unfolded protein response could be key determinants of the differential resistance of MM to VAs.</abstract><note type="additional physical form">Table S1. 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