LUBAC determines chemotherapy resistance in squamous cell lung cancer
Lung squamous cell carcinoma (LSCC) and adenocarcinoma (LADC) are the most common lung cancer subtypes. Molecular targeted treatments have improved LADC patient survival but are largely ineffective in LSCC. The tumor suppressor FBW7 is commonly mutated or down-regulated in human LSCC, and oncogenic...
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| Veröffentlicht in: | The Journal of experimental medicine 2019-02, Vol.216 (2), p.450-465 |
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| creator | Ruiz, E Josue Diefenbacher, Markus E Nelson, Jessica K Sancho, Rocio Pucci, Fabio Chakraborty, Atanu Moreno, Paula Annibaldi, Alessandro Liccardi, Gianmaria Encheva, Vesela Mitter, Richard Rosenfeldt, Mathias Snijders, Ambrosius P Meier, Pascal Calzado, Marco A Behrens, Axel |
| description | Lung squamous cell carcinoma (LSCC) and adenocarcinoma (LADC) are the most common lung cancer subtypes. Molecular targeted treatments have improved LADC patient survival but are largely ineffective in LSCC. The tumor suppressor FBW7 is commonly mutated or down-regulated in human LSCC, and oncogenic
activation combined with
inactivation in mice (KF model) caused both LSCC and LADC. Lineage-tracing experiments showed that CC10
, but not basal, cells are the cells of origin of LSCC in KF mice. KF LSCC tumors recapitulated human LSCC resistance to cisplatin-based chemotherapy, and we identified LUBAC-mediated NF-κB signaling as a determinant of chemotherapy resistance in human and mouse. Inhibition of NF-κB activation using TAK1 or LUBAC inhibitors resensitized LSCC tumors to cisplatin, suggesting a future avenue for LSCC patient treatment. |
| doi_str_mv | 10.1084/jem.20180742 |
| format | Article |
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activation combined with
inactivation in mice (KF model) caused both LSCC and LADC. Lineage-tracing experiments showed that CC10
, but not basal, cells are the cells of origin of LSCC in KF mice. KF LSCC tumors recapitulated human LSCC resistance to cisplatin-based chemotherapy, and we identified LUBAC-mediated NF-κB signaling as a determinant of chemotherapy resistance in human and mouse. Inhibition of NF-κB activation using TAK1 or LUBAC inhibitors resensitized LSCC tumors to cisplatin, suggesting a future avenue for LSCC patient treatment.</description><identifier>ISSN: 0022-1007</identifier><identifier>ISSN: 1540-9538</identifier><identifier>EISSN: 1540-9538</identifier><identifier>DOI: 10.1084/jem.20180742</identifier><identifier>PMID: 30642944</identifier><language>eng</language><publisher>United States: Rockefeller University Press</publisher><subject>Adenocarcinoma of Lung - drug therapy ; Adenocarcinoma of Lung - enzymology ; Adenocarcinoma of Lung - genetics ; Adenocarcinoma of Lung - pathology ; Animals ; Carcinoma, Squamous Cell - drug therapy ; Carcinoma, Squamous Cell - enzymology ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - pathology ; Cisplatin - pharmacology ; Drug Resistance, Neoplasm ; Humans ; Lung Neoplasms - drug therapy ; Lung Neoplasms - enzymology ; Lung Neoplasms - genetics ; Lung Neoplasms - pathology ; Mice ; Multienzyme Complexes - genetics ; Multienzyme Complexes - metabolism ; Proto-Oncogene Proteins p21(ras) - genetics ; Proto-Oncogene Proteins p21(ras) - metabolism ; Ubiquitination</subject><ispartof>The Journal of experimental medicine, 2019-02, Vol.216 (2), p.450-465</ispartof><rights>2019 Ruiz et al.</rights><rights>2019 Ruiz et al. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c450t-3b9b7cd66fa1f118a4d097605d9bbc0d0f0c9178bbcc4117191c205df692446c3</citedby><cites>FETCH-LOGICAL-c450t-3b9b7cd66fa1f118a4d097605d9bbc0d0f0c9178bbcc4117191c205df692446c3</cites><orcidid>0000-0002-4894-5391 ; 0000-0002-1279-3760 ; 0000-0002-1557-1143 ; 0000-0002-5338-535X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30642944$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ruiz, E Josue</creatorcontrib><creatorcontrib>Diefenbacher, Markus E</creatorcontrib><creatorcontrib>Nelson, Jessica K</creatorcontrib><creatorcontrib>Sancho, Rocio</creatorcontrib><creatorcontrib>Pucci, Fabio</creatorcontrib><creatorcontrib>Chakraborty, Atanu</creatorcontrib><creatorcontrib>Moreno, Paula</creatorcontrib><creatorcontrib>Annibaldi, Alessandro</creatorcontrib><creatorcontrib>Liccardi, Gianmaria</creatorcontrib><creatorcontrib>Encheva, Vesela</creatorcontrib><creatorcontrib>Mitter, Richard</creatorcontrib><creatorcontrib>Rosenfeldt, Mathias</creatorcontrib><creatorcontrib>Snijders, Ambrosius P</creatorcontrib><creatorcontrib>Meier, Pascal</creatorcontrib><creatorcontrib>Calzado, Marco A</creatorcontrib><creatorcontrib>Behrens, Axel</creatorcontrib><title>LUBAC determines chemotherapy resistance in squamous cell lung cancer</title><title>The Journal of experimental medicine</title><addtitle>J Exp Med</addtitle><description>Lung squamous cell carcinoma (LSCC) and adenocarcinoma (LADC) are the most common lung cancer subtypes. Molecular targeted treatments have improved LADC patient survival but are largely ineffective in LSCC. The tumor suppressor FBW7 is commonly mutated or down-regulated in human LSCC, and oncogenic
activation combined with
inactivation in mice (KF model) caused both LSCC and LADC. Lineage-tracing experiments showed that CC10
, but not basal, cells are the cells of origin of LSCC in KF mice. KF LSCC tumors recapitulated human LSCC resistance to cisplatin-based chemotherapy, and we identified LUBAC-mediated NF-κB signaling as a determinant of chemotherapy resistance in human and mouse. Inhibition of NF-κB activation using TAK1 or LUBAC inhibitors resensitized LSCC tumors to cisplatin, suggesting a future avenue for LSCC patient treatment.</description><subject>Adenocarcinoma of Lung - drug therapy</subject><subject>Adenocarcinoma of Lung - enzymology</subject><subject>Adenocarcinoma of Lung - genetics</subject><subject>Adenocarcinoma of Lung - pathology</subject><subject>Animals</subject><subject>Carcinoma, Squamous Cell - drug therapy</subject><subject>Carcinoma, Squamous Cell - enzymology</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Cisplatin - pharmacology</subject><subject>Drug Resistance, Neoplasm</subject><subject>Humans</subject><subject>Lung Neoplasms - drug therapy</subject><subject>Lung Neoplasms - enzymology</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - pathology</subject><subject>Mice</subject><subject>Multienzyme Complexes - genetics</subject><subject>Multienzyme Complexes - metabolism</subject><subject>Proto-Oncogene Proteins p21(ras) - genetics</subject><subject>Proto-Oncogene Proteins p21(ras) - metabolism</subject><subject>Ubiquitination</subject><issn>0022-1007</issn><issn>1540-9538</issn><issn>1540-9538</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkMtOwzAQRS0EoqWwY42yZEHKjOM48QapVOUhVWJD15bjOG2qPFo7Qerf46oPwcoa3aM7nkPIPcIYIWXPa1OPKWAKCaMXZIgxg1DEUXpJhgCUhgiQDMiNc2sAZCzm12QQAWdUMDYks_nidTINctMZW5eNcYFembrtVsaqzS6wxpWuU402QdkEbturuu09Y6oqqPpmGeh9Zm_JVaEqZ-6O74gs3mbf049w_vX-OZ3MQ81i6MIoE1mic84LhQViqlgOIuEQ5yLLNORQgBaYpH7QDDFBgZr6tOCCMsZ1NCIvh95Nn9Um16bprKrkxpa1sjvZqlL-T5pyJZftj-QRjxhNfcHjscC22964Ttal21-jGuMPkxQTEcVeGfXo0wHVtnXOmuK8BkHuzUtvXp7Me_zh79fO8El19AvMCH-q</recordid><startdate>20190204</startdate><enddate>20190204</enddate><creator>Ruiz, E Josue</creator><creator>Diefenbacher, Markus E</creator><creator>Nelson, Jessica K</creator><creator>Sancho, Rocio</creator><creator>Pucci, Fabio</creator><creator>Chakraborty, Atanu</creator><creator>Moreno, Paula</creator><creator>Annibaldi, Alessandro</creator><creator>Liccardi, Gianmaria</creator><creator>Encheva, Vesela</creator><creator>Mitter, Richard</creator><creator>Rosenfeldt, Mathias</creator><creator>Snijders, Ambrosius P</creator><creator>Meier, Pascal</creator><creator>Calzado, Marco A</creator><creator>Behrens, Axel</creator><general>Rockefeller University Press</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-4894-5391</orcidid><orcidid>https://orcid.org/0000-0002-1279-3760</orcidid><orcidid>https://orcid.org/0000-0002-1557-1143</orcidid><orcidid>https://orcid.org/0000-0002-5338-535X</orcidid></search><sort><creationdate>20190204</creationdate><title>LUBAC determines chemotherapy resistance in squamous cell lung cancer</title><author>Ruiz, E Josue ; Diefenbacher, Markus E ; Nelson, Jessica K ; Sancho, Rocio ; Pucci, Fabio ; Chakraborty, Atanu ; Moreno, Paula ; Annibaldi, Alessandro ; Liccardi, Gianmaria ; Encheva, Vesela ; Mitter, Richard ; Rosenfeldt, Mathias ; Snijders, Ambrosius P ; Meier, Pascal ; Calzado, Marco A ; Behrens, Axel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c450t-3b9b7cd66fa1f118a4d097605d9bbc0d0f0c9178bbcc4117191c205df692446c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adenocarcinoma of Lung - drug therapy</topic><topic>Adenocarcinoma of Lung - enzymology</topic><topic>Adenocarcinoma of Lung - genetics</topic><topic>Adenocarcinoma of Lung - pathology</topic><topic>Animals</topic><topic>Carcinoma, Squamous Cell - drug therapy</topic><topic>Carcinoma, Squamous Cell - enzymology</topic><topic>Carcinoma, Squamous Cell - genetics</topic><topic>Carcinoma, Squamous Cell - pathology</topic><topic>Cisplatin - pharmacology</topic><topic>Drug Resistance, Neoplasm</topic><topic>Humans</topic><topic>Lung Neoplasms - drug therapy</topic><topic>Lung Neoplasms - enzymology</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - pathology</topic><topic>Mice</topic><topic>Multienzyme Complexes - genetics</topic><topic>Multienzyme Complexes - metabolism</topic><topic>Proto-Oncogene Proteins p21(ras) - genetics</topic><topic>Proto-Oncogene Proteins p21(ras) - metabolism</topic><topic>Ubiquitination</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ruiz, E Josue</creatorcontrib><creatorcontrib>Diefenbacher, Markus E</creatorcontrib><creatorcontrib>Nelson, Jessica K</creatorcontrib><creatorcontrib>Sancho, Rocio</creatorcontrib><creatorcontrib>Pucci, Fabio</creatorcontrib><creatorcontrib>Chakraborty, Atanu</creatorcontrib><creatorcontrib>Moreno, Paula</creatorcontrib><creatorcontrib>Annibaldi, Alessandro</creatorcontrib><creatorcontrib>Liccardi, Gianmaria</creatorcontrib><creatorcontrib>Encheva, Vesela</creatorcontrib><creatorcontrib>Mitter, Richard</creatorcontrib><creatorcontrib>Rosenfeldt, Mathias</creatorcontrib><creatorcontrib>Snijders, Ambrosius P</creatorcontrib><creatorcontrib>Meier, Pascal</creatorcontrib><creatorcontrib>Calzado, Marco A</creatorcontrib><creatorcontrib>Behrens, Axel</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of experimental medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ruiz, E Josue</au><au>Diefenbacher, Markus E</au><au>Nelson, Jessica K</au><au>Sancho, Rocio</au><au>Pucci, Fabio</au><au>Chakraborty, Atanu</au><au>Moreno, Paula</au><au>Annibaldi, Alessandro</au><au>Liccardi, Gianmaria</au><au>Encheva, Vesela</au><au>Mitter, Richard</au><au>Rosenfeldt, Mathias</au><au>Snijders, Ambrosius P</au><au>Meier, Pascal</au><au>Calzado, Marco A</au><au>Behrens, Axel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LUBAC determines chemotherapy resistance in squamous cell lung cancer</atitle><jtitle>The Journal of experimental medicine</jtitle><addtitle>J Exp Med</addtitle><date>2019-02-04</date><risdate>2019</risdate><volume>216</volume><issue>2</issue><spage>450</spage><epage>465</epage><pages>450-465</pages><issn>0022-1007</issn><issn>1540-9538</issn><eissn>1540-9538</eissn><abstract>Lung squamous cell carcinoma (LSCC) and adenocarcinoma (LADC) are the most common lung cancer subtypes. Molecular targeted treatments have improved LADC patient survival but are largely ineffective in LSCC. The tumor suppressor FBW7 is commonly mutated or down-regulated in human LSCC, and oncogenic
activation combined with
inactivation in mice (KF model) caused both LSCC and LADC. Lineage-tracing experiments showed that CC10
, but not basal, cells are the cells of origin of LSCC in KF mice. KF LSCC tumors recapitulated human LSCC resistance to cisplatin-based chemotherapy, and we identified LUBAC-mediated NF-κB signaling as a determinant of chemotherapy resistance in human and mouse. Inhibition of NF-κB activation using TAK1 or LUBAC inhibitors resensitized LSCC tumors to cisplatin, suggesting a future avenue for LSCC patient treatment.</abstract><cop>United States</cop><pub>Rockefeller University Press</pub><pmid>30642944</pmid><doi>10.1084/jem.20180742</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0002-4894-5391</orcidid><orcidid>https://orcid.org/0000-0002-1279-3760</orcidid><orcidid>https://orcid.org/0000-0002-1557-1143</orcidid><orcidid>https://orcid.org/0000-0002-5338-535X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adenocarcinoma of Lung - drug therapy Adenocarcinoma of Lung - enzymology Adenocarcinoma of Lung - genetics Adenocarcinoma of Lung - pathology Animals Carcinoma, Squamous Cell - drug therapy Carcinoma, Squamous Cell - enzymology Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - pathology Cisplatin - pharmacology Drug Resistance, Neoplasm Humans Lung Neoplasms - drug therapy Lung Neoplasms - enzymology Lung Neoplasms - genetics Lung Neoplasms - pathology Mice Multienzyme Complexes - genetics Multienzyme Complexes - metabolism Proto-Oncogene Proteins p21(ras) - genetics Proto-Oncogene Proteins p21(ras) - metabolism Ubiquitination |
| title | LUBAC determines chemotherapy resistance in squamous cell lung cancer |
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