Pro-apoptotic effect of Δ2-TGZ in “claudin-1-low” triple-negative breast cancer cells: involvement of claudin-1
Purpose 40% of triple-negative breast cancer (TNBC) do not express claudin-1, a major constituent of tight junction. Patients with these “claudin-1-low” tumors present a higher relapse incidence. A major challenge in oncology is the development of innovative therapies for such poor prognosis tumors....
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| Veröffentlicht in: | Breast cancer research and treatment 2017-10, Vol.165 (3), p.517-527 |
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| creator | Geoffroy, Marine Kleinclauss, Alexandra Grandemange, Stéphanie Hupont, Sébastien Boisbrun, Michel Flament, Stéphane Grillier-Vuissoz, Isabelle Kuntz, Sandra |
| description | Purpose
40% of triple-negative breast cancer (TNBC) do not express claudin-1, a major constituent of tight junction. Patients with these “claudin-1-low” tumors present a higher relapse incidence. A major challenge in oncology is the development of innovative therapies for such poor prognosis tumors. In this context, we study the anticancer effects of ∆2-TGZ, a compound derived from troglitazone (TGZ), on cell models of these tumors.
Methods and results
In MDA-MB-231 and Hs578T “claudin-1-low” TNBC cells, Δ2-TGZ treatment induced claudin-1 protein expression and triggered apoptosis as measured by FACS analysis (annexin V/PI co-staining). Interestingly, in the non-tumorigenic human breast epithelial cell line MCF-10A, the basal level of claudin-1 was not modified following Δ2-TGZ treatment, which did not induce apoptosis. Furthermore, claudin-1-transfected MDA-MB-231 and Hs578T cells displayed a significant increase of cleaved PARP-1 and caspase 7, caspase 3/7 activities, and TUNEL staining. RNA interference was performed in order to inhibit Δ2-TGZ-induced claudin-1 expression in both the cells. In absence of claudin-1, a decrease of cleaved PARP-1 and caspase 7 and caspase 3/7 activities were observed in MDA-MB-231 but not in Hs578T cells.
Conclusion
Claudin-1 overexpression and Δ2-TGZ treatment are associated to apoptosis in MDA-MB-231 and Hs578T “claudin-1-low” TNBC. Moreover, in MDA-MB-231 cells, claudin-1 is involved in the pro-apoptotic effect of Δ2-TGZ. Our results suggest that claudin-1 re-expression could be an interesting therapeutic strategy for “claudin-1-low” TNBC. |
| doi_str_mv | 10.1007/s10549-017-4378-2 |
| format | Article |
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40% of triple-negative breast cancer (TNBC) do not express claudin-1, a major constituent of tight junction. Patients with these “claudin-1-low” tumors present a higher relapse incidence. A major challenge in oncology is the development of innovative therapies for such poor prognosis tumors. In this context, we study the anticancer effects of ∆2-TGZ, a compound derived from troglitazone (TGZ), on cell models of these tumors.
Methods and results
In MDA-MB-231 and Hs578T “claudin-1-low” TNBC cells, Δ2-TGZ treatment induced claudin-1 protein expression and triggered apoptosis as measured by FACS analysis (annexin V/PI co-staining). Interestingly, in the non-tumorigenic human breast epithelial cell line MCF-10A, the basal level of claudin-1 was not modified following Δ2-TGZ treatment, which did not induce apoptosis. Furthermore, claudin-1-transfected MDA-MB-231 and Hs578T cells displayed a significant increase of cleaved PARP-1 and caspase 7, caspase 3/7 activities, and TUNEL staining. RNA interference was performed in order to inhibit Δ2-TGZ-induced claudin-1 expression in both the cells. In absence of claudin-1, a decrease of cleaved PARP-1 and caspase 7 and caspase 3/7 activities were observed in MDA-MB-231 but not in Hs578T cells.
Conclusion
Claudin-1 overexpression and Δ2-TGZ treatment are associated to apoptosis in MDA-MB-231 and Hs578T “claudin-1-low” TNBC. Moreover, in MDA-MB-231 cells, claudin-1 is involved in the pro-apoptotic effect of Δ2-TGZ. Our results suggest that claudin-1 re-expression could be an interesting therapeutic strategy for “claudin-1-low” TNBC.</description><identifier>ISSN: 0167-6806</identifier><identifier>EISSN: 1573-7217</identifier><identifier>DOI: 10.1007/s10549-017-4378-2</identifier><identifier>PMID: 28681173</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Annexin V ; Apoptosis ; Breast cancer ; Cancer ; Cancer research ; Caspase ; Caspase-3 ; Caspase-7 ; Cell culture ; Epithelial cells ; Flow cytometry ; Life Sciences ; Medical innovations ; Medicine ; Medicine & Public Health ; Oncology ; Poly(ADP-ribose) polymerase ; Preclinical Study ; RNA-mediated interference ; Troglitazone ; Tumors</subject><ispartof>Breast cancer research and treatment, 2017-10, Vol.165 (3), p.517-527</ispartof><rights>Springer Science+Business Media, LLC 2017</rights><rights>Breast Cancer Research and Treatment is a copyright of Springer, 2017.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c406t-886a9bafecfacc0e0d2abf4a61980b1360595f608d06d1a1722312d45bcac3a23</citedby><cites>FETCH-LOGICAL-c406t-886a9bafecfacc0e0d2abf4a61980b1360595f608d06d1a1722312d45bcac3a23</cites><orcidid>0000-0002-9820-3804 ; 0000-0002-9162-1288 ; 0000-0003-4766-1175 ; 0000-0001-6588-0027 ; 0000-0002-0015-2712 ; 0000-0002-4101-6303</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10549-017-4378-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10549-017-4378-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,780,784,885,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28681173$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-01589665$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Geoffroy, Marine</creatorcontrib><creatorcontrib>Kleinclauss, Alexandra</creatorcontrib><creatorcontrib>Grandemange, Stéphanie</creatorcontrib><creatorcontrib>Hupont, Sébastien</creatorcontrib><creatorcontrib>Boisbrun, Michel</creatorcontrib><creatorcontrib>Flament, Stéphane</creatorcontrib><creatorcontrib>Grillier-Vuissoz, Isabelle</creatorcontrib><creatorcontrib>Kuntz, Sandra</creatorcontrib><title>Pro-apoptotic effect of Δ2-TGZ in “claudin-1-low” triple-negative breast cancer cells: involvement of claudin-1</title><title>Breast cancer research and treatment</title><addtitle>Breast Cancer Res Treat</addtitle><addtitle>Breast Cancer Res Treat</addtitle><description>Purpose
40% of triple-negative breast cancer (TNBC) do not express claudin-1, a major constituent of tight junction. Patients with these “claudin-1-low” tumors present a higher relapse incidence. A major challenge in oncology is the development of innovative therapies for such poor prognosis tumors. In this context, we study the anticancer effects of ∆2-TGZ, a compound derived from troglitazone (TGZ), on cell models of these tumors.
Methods and results
In MDA-MB-231 and Hs578T “claudin-1-low” TNBC cells, Δ2-TGZ treatment induced claudin-1 protein expression and triggered apoptosis as measured by FACS analysis (annexin V/PI co-staining). Interestingly, in the non-tumorigenic human breast epithelial cell line MCF-10A, the basal level of claudin-1 was not modified following Δ2-TGZ treatment, which did not induce apoptosis. Furthermore, claudin-1-transfected MDA-MB-231 and Hs578T cells displayed a significant increase of cleaved PARP-1 and caspase 7, caspase 3/7 activities, and TUNEL staining. RNA interference was performed in order to inhibit Δ2-TGZ-induced claudin-1 expression in both the cells. In absence of claudin-1, a decrease of cleaved PARP-1 and caspase 7 and caspase 3/7 activities were observed in MDA-MB-231 but not in Hs578T cells.
Conclusion
Claudin-1 overexpression and Δ2-TGZ treatment are associated to apoptosis in MDA-MB-231 and Hs578T “claudin-1-low” TNBC. Moreover, in MDA-MB-231 cells, claudin-1 is involved in the pro-apoptotic effect of Δ2-TGZ. Our results suggest that claudin-1 re-expression could be an interesting therapeutic strategy for “claudin-1-low” TNBC.</description><subject>Annexin V</subject><subject>Apoptosis</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Cancer research</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Caspase-7</subject><subject>Cell culture</subject><subject>Epithelial cells</subject><subject>Flow cytometry</subject><subject>Life Sciences</subject><subject>Medical innovations</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Oncology</subject><subject>Poly(ADP-ribose) polymerase</subject><subject>Preclinical Study</subject><subject>RNA-mediated interference</subject><subject>Troglitazone</subject><subject>Tumors</subject><issn>0167-6806</issn><issn>1573-7217</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1kUFu1TAQhi0Eoo_CAdggS2xgYZhxEtthV1XQIj0JFmXDxnIcp6TKi4PtPMSuh2AJV-IQPQkOKU8IiZWl8Tf__DM_IY8RXiCAfBkRqrJmgJKVhVSM3yEbrGTBJEd5l2wAhWRCgTgiD2K8AoBaQn2fHHElFKIsNiS9D56ZyU_Jp95S13XOJuo7-vMbZxdnH2k_0pvr73Ywc9uPDNngv9xc_6Ap9NPg2OguTer3jjbBmZioNaN1gVo3DPFV7t37Ye92bvwteRB5SO51Zoju0e17TD68eX1xes62787enp5smS1BJKaUMHVjsqPOWAsOWm6arjQCawUNFgKquuoEqBZEiwYl5wXytqwaa2xheHFMnq-6n8ygp9DvTPiqven1-clWLzXAStVCVHvM7LOVnYL_PLuY9K6Pyx5mdH6OGut8TERVqIw-_Qe98nMY8yaZKmuBnJcyU7hSNvgYg-sODhD0Ep9e48smpF7i04vhJ7fKc7Nz7aHjT14Z4CsQ89d46cJfo_-r-gu1PKZB</recordid><startdate>20171001</startdate><enddate>20171001</enddate><creator>Geoffroy, Marine</creator><creator>Kleinclauss, Alexandra</creator><creator>Grandemange, Stéphanie</creator><creator>Hupont, Sébastien</creator><creator>Boisbrun, Michel</creator><creator>Flament, Stéphane</creator><creator>Grillier-Vuissoz, Isabelle</creator><creator>Kuntz, Sandra</creator><general>Springer US</general><general>Springer Nature B.V</general><general>Springer Verlag</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9-</scope><scope>K9.</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0002-9820-3804</orcidid><orcidid>https://orcid.org/0000-0002-9162-1288</orcidid><orcidid>https://orcid.org/0000-0003-4766-1175</orcidid><orcidid>https://orcid.org/0000-0001-6588-0027</orcidid><orcidid>https://orcid.org/0000-0002-0015-2712</orcidid><orcidid>https://orcid.org/0000-0002-4101-6303</orcidid></search><sort><creationdate>20171001</creationdate><title>Pro-apoptotic effect of Δ2-TGZ in “claudin-1-low” triple-negative breast cancer cells: involvement of claudin-1</title><author>Geoffroy, Marine ; Kleinclauss, Alexandra ; Grandemange, Stéphanie ; Hupont, Sébastien ; Boisbrun, Michel ; Flament, Stéphane ; Grillier-Vuissoz, Isabelle ; Kuntz, Sandra</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c406t-886a9bafecfacc0e0d2abf4a61980b1360595f608d06d1a1722312d45bcac3a23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Annexin V</topic><topic>Apoptosis</topic><topic>Breast cancer</topic><topic>Cancer</topic><topic>Cancer research</topic><topic>Caspase</topic><topic>Caspase-3</topic><topic>Caspase-7</topic><topic>Cell culture</topic><topic>Epithelial cells</topic><topic>Flow cytometry</topic><topic>Life Sciences</topic><topic>Medical innovations</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Oncology</topic><topic>Poly(ADP-ribose) polymerase</topic><topic>Preclinical Study</topic><topic>RNA-mediated interference</topic><topic>Troglitazone</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Geoffroy, Marine</creatorcontrib><creatorcontrib>Kleinclauss, Alexandra</creatorcontrib><creatorcontrib>Grandemange, Stéphanie</creatorcontrib><creatorcontrib>Hupont, Sébastien</creatorcontrib><creatorcontrib>Boisbrun, Michel</creatorcontrib><creatorcontrib>Flament, Stéphane</creatorcontrib><creatorcontrib>Grillier-Vuissoz, Isabelle</creatorcontrib><creatorcontrib>Kuntz, Sandra</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Breast cancer research and treatment</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Geoffroy, Marine</au><au>Kleinclauss, Alexandra</au><au>Grandemange, Stéphanie</au><au>Hupont, Sébastien</au><au>Boisbrun, Michel</au><au>Flament, Stéphane</au><au>Grillier-Vuissoz, Isabelle</au><au>Kuntz, Sandra</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pro-apoptotic effect of Δ2-TGZ in “claudin-1-low” triple-negative breast cancer cells: involvement of claudin-1</atitle><jtitle>Breast cancer research and treatment</jtitle><stitle>Breast Cancer Res Treat</stitle><addtitle>Breast Cancer Res Treat</addtitle><date>2017-10-01</date><risdate>2017</risdate><volume>165</volume><issue>3</issue><spage>517</spage><epage>527</epage><pages>517-527</pages><issn>0167-6806</issn><eissn>1573-7217</eissn><abstract>Purpose
40% of triple-negative breast cancer (TNBC) do not express claudin-1, a major constituent of tight junction. Patients with these “claudin-1-low” tumors present a higher relapse incidence. A major challenge in oncology is the development of innovative therapies for such poor prognosis tumors. In this context, we study the anticancer effects of ∆2-TGZ, a compound derived from troglitazone (TGZ), on cell models of these tumors.
Methods and results
In MDA-MB-231 and Hs578T “claudin-1-low” TNBC cells, Δ2-TGZ treatment induced claudin-1 protein expression and triggered apoptosis as measured by FACS analysis (annexin V/PI co-staining). Interestingly, in the non-tumorigenic human breast epithelial cell line MCF-10A, the basal level of claudin-1 was not modified following Δ2-TGZ treatment, which did not induce apoptosis. Furthermore, claudin-1-transfected MDA-MB-231 and Hs578T cells displayed a significant increase of cleaved PARP-1 and caspase 7, caspase 3/7 activities, and TUNEL staining. RNA interference was performed in order to inhibit Δ2-TGZ-induced claudin-1 expression in both the cells. In absence of claudin-1, a decrease of cleaved PARP-1 and caspase 7 and caspase 3/7 activities were observed in MDA-MB-231 but not in Hs578T cells.
Conclusion
Claudin-1 overexpression and Δ2-TGZ treatment are associated to apoptosis in MDA-MB-231 and Hs578T “claudin-1-low” TNBC. Moreover, in MDA-MB-231 cells, claudin-1 is involved in the pro-apoptotic effect of Δ2-TGZ. Our results suggest that claudin-1 re-expression could be an interesting therapeutic strategy for “claudin-1-low” TNBC.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>28681173</pmid><doi>10.1007/s10549-017-4378-2</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-9820-3804</orcidid><orcidid>https://orcid.org/0000-0002-9162-1288</orcidid><orcidid>https://orcid.org/0000-0003-4766-1175</orcidid><orcidid>https://orcid.org/0000-0001-6588-0027</orcidid><orcidid>https://orcid.org/0000-0002-0015-2712</orcidid><orcidid>https://orcid.org/0000-0002-4101-6303</orcidid></addata></record> |
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| ispartof | Breast cancer research and treatment, 2017-10, Vol.165 (3), p.517-527 |
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| source | SpringerLink Journals - AutoHoldings |
| subjects | Annexin V Apoptosis Breast cancer Cancer Cancer research Caspase Caspase-3 Caspase-7 Cell culture Epithelial cells Flow cytometry Life Sciences Medical innovations Medicine Medicine & Public Health Oncology Poly(ADP-ribose) polymerase Preclinical Study RNA-mediated interference Troglitazone Tumors |
| title | Pro-apoptotic effect of Δ2-TGZ in “claudin-1-low” triple-negative breast cancer cells: involvement of claudin-1 |
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