Epithelial-to-mesenchymal transition hinders interferon-γ-dependent immunosurveillance in lung cancer cells
The epithelial-to-mesenchymal transition (EMT) is involved in cancer metastasis; nevertheless, interferon (IFN)-γ induces anticancer activities by causing cell growth suppression, cytotoxicity, and migration inhibition. Regarding the poor response to exogenously administered IFN-γ as anticancer ther...
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| Veröffentlicht in: | Cancer letters 2022-07, Vol.539, p.215712-215712, Article 215712 |
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| creator | Tseng, Po-Chun Chen, Chia-Ling Lee, Kang-Yuan Feng, Po-Hao Wang, Yu-Chih Satria, Rahmat Dani Lin, Chiou-Feng |
| description | The epithelial-to-mesenchymal transition (EMT) is involved in cancer metastasis; nevertheless, interferon (IFN)-γ induces anticancer activities by causing cell growth suppression, cytotoxicity, and migration inhibition. Regarding the poor response to exogenously administered IFN-γ as anticancer therapy, it was hypothesized that malignant cells may acquire a means of escaping from IFN-γ immunosurveillance, likely through an EMT-related process. A genomic analysis of human lung cancers revealed a negative link between the EMT and IFN-γ signaling, while compared to human lung adenocarcinoma A549 cells, IFN-γ-hyporesponsive AS2 cells exhibited mesenchymal characteristics. Chemically, physically, and genetically engineered EMT attenuated IFN-γ-induced IFN regulatory factor 1 transactivation. Poststimulation of transforming growth factor-β induced the EMT and also selectively retarded IFN-γ-responsive gene expression as well as IFN-γ-induced signal transducer and activator of transcription 1 activation, major histocompatibility complex I, and CD54 expression, cell migration/invasion inhibition, and direct/indirect cytotoxicity. Without changes in IFN-γ receptors, excessive oxidative activation of Src homology-2 containing phosphatase 2 (SHP2) in cells undergoing the EMT primarily caused cellular hyporesponsiveness to IFN-γ signaling and cytotoxicity, while combining an SHP2 inhibitor or antioxidant sensitized EMT-associated AS2 and mesenchymal A549 cells to IFN-γ-induced priming effects on tumor necrosis factor-related apoptosis-inducing ligand cytotoxicity. In cell line-derived xenograft models, combined treatment with IFN-γ and an SHP2 inhibitor induced enhanced anticancer activities. These results imply that EMT-associated SHP2 activation inhibits IFN-γ signaling, facilitating lung cancer cell escape from IFN-γ immunosurveillance.
•The malignant lung cancer cells acquire EMT to escape from IFN-γ immunosurveillance.•SHP2 in EMT cells determine cellular hyporesponsiveness to IFN-γ signaling and cytotoxicity.•Combined treatment with IFN-γ and an SHP2 inhibitor induced enhances anticancer therapy in vitro and in vivo. |
| doi_str_mv | 10.1016/j.canlet.2022.215712 |
| format | Article |
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•The malignant lung cancer cells acquire EMT to escape from IFN-γ immunosurveillance.•SHP2 in EMT cells determine cellular hyporesponsiveness to IFN-γ signaling and cytotoxicity.•Combined treatment with IFN-γ and an SHP2 inhibitor induced enhances anticancer therapy in vitro and in vivo.</description><identifier>ISSN: 0304-3835</identifier><identifier>EISSN: 1872-7980</identifier><identifier>DOI: 10.1016/j.canlet.2022.215712</identifier><identifier>PMID: 35490920</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><subject>Adenocarcinoma ; Antioxidants ; Apoptosis ; Cell adhesion & migration ; Cell culture ; Cell Line, Tumor ; Cell migration ; Cell Movement - immunology ; Cytokines ; Cytotoxicity ; EMT ; Epithelial-Mesenchymal Transition - immunology ; Gene expression ; Genetic engineering ; Genomic analysis ; Growth factors ; Homology ; Humans ; Hypoxia ; IFN-γ ; Immunologic Surveillance ; Immunosurveillance ; Interferon-gamma - immunology ; Interferon-gamma - pharmacology ; Kinases ; Lung cancer ; Lung Neoplasms - drug therapy ; Lung Neoplasms - genetics ; Lung Neoplasms - immunology ; Lung Neoplasms - pathology ; Major histocompatibility complex ; Mesenchyme ; Metastases ; Metastasis ; MHC ; Migration inhibition ; Monoclonal antibodies ; Morphology ; Phosphatase ; Proteins ; Software ; STAT1 ; TRAIL protein ; Transcription activation ; Tumor necrosis factor-TNF ; Xenografts ; γ-Interferon</subject><ispartof>Cancer letters, 2022-07, Vol.539, p.215712-215712, Article 215712</ispartof><rights>2022 Elsevier B.V.</rights><rights>Copyright © 2022 Elsevier B.V. All rights reserved.</rights><rights>2022. Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c305t-afa7513af17ac38608269b2ca2d9e54d19cd81d414128b499db21275464b0c513</citedby><cites>FETCH-LOGICAL-c305t-afa7513af17ac38608269b2ca2d9e54d19cd81d414128b499db21275464b0c513</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0304383522001963$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35490920$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tseng, Po-Chun</creatorcontrib><creatorcontrib>Chen, Chia-Ling</creatorcontrib><creatorcontrib>Lee, Kang-Yuan</creatorcontrib><creatorcontrib>Feng, Po-Hao</creatorcontrib><creatorcontrib>Wang, Yu-Chih</creatorcontrib><creatorcontrib>Satria, Rahmat Dani</creatorcontrib><creatorcontrib>Lin, Chiou-Feng</creatorcontrib><title>Epithelial-to-mesenchymal transition hinders interferon-γ-dependent immunosurveillance in lung cancer cells</title><title>Cancer letters</title><addtitle>Cancer Lett</addtitle><description>The epithelial-to-mesenchymal transition (EMT) is involved in cancer metastasis; nevertheless, interferon (IFN)-γ induces anticancer activities by causing cell growth suppression, cytotoxicity, and migration inhibition. Regarding the poor response to exogenously administered IFN-γ as anticancer therapy, it was hypothesized that malignant cells may acquire a means of escaping from IFN-γ immunosurveillance, likely through an EMT-related process. A genomic analysis of human lung cancers revealed a negative link between the EMT and IFN-γ signaling, while compared to human lung adenocarcinoma A549 cells, IFN-γ-hyporesponsive AS2 cells exhibited mesenchymal characteristics. Chemically, physically, and genetically engineered EMT attenuated IFN-γ-induced IFN regulatory factor 1 transactivation. Poststimulation of transforming growth factor-β induced the EMT and also selectively retarded IFN-γ-responsive gene expression as well as IFN-γ-induced signal transducer and activator of transcription 1 activation, major histocompatibility complex I, and CD54 expression, cell migration/invasion inhibition, and direct/indirect cytotoxicity. Without changes in IFN-γ receptors, excessive oxidative activation of Src homology-2 containing phosphatase 2 (SHP2) in cells undergoing the EMT primarily caused cellular hyporesponsiveness to IFN-γ signaling and cytotoxicity, while combining an SHP2 inhibitor or antioxidant sensitized EMT-associated AS2 and mesenchymal A549 cells to IFN-γ-induced priming effects on tumor necrosis factor-related apoptosis-inducing ligand cytotoxicity. In cell line-derived xenograft models, combined treatment with IFN-γ and an SHP2 inhibitor induced enhanced anticancer activities. These results imply that EMT-associated SHP2 activation inhibits IFN-γ signaling, facilitating lung cancer cell escape from IFN-γ immunosurveillance.
•The malignant lung cancer cells acquire EMT to escape from IFN-γ immunosurveillance.•SHP2 in EMT cells determine cellular hyporesponsiveness to IFN-γ signaling and cytotoxicity.•Combined treatment with IFN-γ and an SHP2 inhibitor induced enhances anticancer therapy in vitro and in vivo.</description><subject>Adenocarcinoma</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Cell adhesion & migration</subject><subject>Cell culture</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement - immunology</subject><subject>Cytokines</subject><subject>Cytotoxicity</subject><subject>EMT</subject><subject>Epithelial-Mesenchymal Transition - immunology</subject><subject>Gene expression</subject><subject>Genetic engineering</subject><subject>Genomic analysis</subject><subject>Growth factors</subject><subject>Homology</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>IFN-γ</subject><subject>Immunologic Surveillance</subject><subject>Immunosurveillance</subject><subject>Interferon-gamma - immunology</subject><subject>Interferon-gamma - pharmacology</subject><subject>Kinases</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - drug therapy</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - immunology</subject><subject>Lung Neoplasms - pathology</subject><subject>Major histocompatibility complex</subject><subject>Mesenchyme</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>MHC</subject><subject>Migration inhibition</subject><subject>Monoclonal antibodies</subject><subject>Morphology</subject><subject>Phosphatase</subject><subject>Proteins</subject><subject>Software</subject><subject>STAT1</subject><subject>TRAIL protein</subject><subject>Transcription activation</subject><subject>Tumor necrosis factor-TNF</subject><subject>Xenografts</subject><subject>γ-Interferon</subject><issn>0304-3835</issn><issn>1872-7980</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kcGOFCEURYnROO3oHxhTiRs3tEBBFWxMzGR0TCZxo2tCwSubDgUtUJPMd_kffpN0anThYlYEcu7j5R6EXlOyp4QO7497a2KAumeEsT2jYqTsCdpROTI8Kkmeoh3pCce97MUFelHKkRAi-Cieo4tecEUUIzsUrk--HiB4E3BNeIEC0R7uFxO6mk0svvoUu4OPDnLpfKyQZ8gp4t-_sIMTtPdYO78sa0xlzXfgQzDRQkO7sMYfnT3fcmchhPISPZtNKPDq4bxE3z9df7u6wbdfP3-5-niLbU9ExWY2o6C9melobC8HItmgJmYNcwoEd1RZJ6njlFMmJ66Umxhlo-ADn4htyUv0bpt7yunnCqXqxZfzBiZCWotmg5ADH5niDX37H3pMa45tu0YNvBVNZN8ovlE2p1IyzPqU_WLyvaZEn23oo95s6LMNvdlosTcPw9dpAfcv9Lf-BnzYAGht3HnIuljfBIDzGWzVLvnHf_gDN6mejg</recordid><startdate>20220728</startdate><enddate>20220728</enddate><creator>Tseng, Po-Chun</creator><creator>Chen, Chia-Ling</creator><creator>Lee, Kang-Yuan</creator><creator>Feng, Po-Hao</creator><creator>Wang, Yu-Chih</creator><creator>Satria, Rahmat Dani</creator><creator>Lin, Chiou-Feng</creator><general>Elsevier B.V</general><general>Elsevier Limited</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>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>20220728</creationdate><title>Epithelial-to-mesenchymal transition hinders interferon-γ-dependent immunosurveillance in lung cancer cells</title><author>Tseng, Po-Chun ; Chen, Chia-Ling ; Lee, Kang-Yuan ; Feng, Po-Hao ; Wang, Yu-Chih ; Satria, Rahmat Dani ; Lin, Chiou-Feng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c305t-afa7513af17ac38608269b2ca2d9e54d19cd81d414128b499db21275464b0c513</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Adenocarcinoma</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Cell adhesion & migration</topic><topic>Cell culture</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement - immunology</topic><topic>Cytokines</topic><topic>Cytotoxicity</topic><topic>EMT</topic><topic>Epithelial-Mesenchymal Transition - immunology</topic><topic>Gene expression</topic><topic>Genetic engineering</topic><topic>Genomic analysis</topic><topic>Growth factors</topic><topic>Homology</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>IFN-γ</topic><topic>Immunologic Surveillance</topic><topic>Immunosurveillance</topic><topic>Interferon-gamma - immunology</topic><topic>Interferon-gamma - pharmacology</topic><topic>Kinases</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - drug therapy</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - immunology</topic><topic>Lung Neoplasms - pathology</topic><topic>Major histocompatibility complex</topic><topic>Mesenchyme</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>MHC</topic><topic>Migration inhibition</topic><topic>Monoclonal antibodies</topic><topic>Morphology</topic><topic>Phosphatase</topic><topic>Proteins</topic><topic>Software</topic><topic>STAT1</topic><topic>TRAIL protein</topic><topic>Transcription activation</topic><topic>Tumor necrosis factor-TNF</topic><topic>Xenografts</topic><topic>γ-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tseng, Po-Chun</creatorcontrib><creatorcontrib>Chen, Chia-Ling</creatorcontrib><creatorcontrib>Lee, Kang-Yuan</creatorcontrib><creatorcontrib>Feng, Po-Hao</creatorcontrib><creatorcontrib>Wang, Yu-Chih</creatorcontrib><creatorcontrib>Satria, Rahmat Dani</creatorcontrib><creatorcontrib>Lin, Chiou-Feng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tseng, Po-Chun</au><au>Chen, Chia-Ling</au><au>Lee, Kang-Yuan</au><au>Feng, Po-Hao</au><au>Wang, Yu-Chih</au><au>Satria, Rahmat Dani</au><au>Lin, Chiou-Feng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Epithelial-to-mesenchymal transition hinders interferon-γ-dependent immunosurveillance in lung cancer cells</atitle><jtitle>Cancer letters</jtitle><addtitle>Cancer Lett</addtitle><date>2022-07-28</date><risdate>2022</risdate><volume>539</volume><spage>215712</spage><epage>215712</epage><pages>215712-215712</pages><artnum>215712</artnum><issn>0304-3835</issn><eissn>1872-7980</eissn><abstract>The epithelial-to-mesenchymal transition (EMT) is involved in cancer metastasis; nevertheless, interferon (IFN)-γ induces anticancer activities by causing cell growth suppression, cytotoxicity, and migration inhibition. Regarding the poor response to exogenously administered IFN-γ as anticancer therapy, it was hypothesized that malignant cells may acquire a means of escaping from IFN-γ immunosurveillance, likely through an EMT-related process. A genomic analysis of human lung cancers revealed a negative link between the EMT and IFN-γ signaling, while compared to human lung adenocarcinoma A549 cells, IFN-γ-hyporesponsive AS2 cells exhibited mesenchymal characteristics. Chemically, physically, and genetically engineered EMT attenuated IFN-γ-induced IFN regulatory factor 1 transactivation. Poststimulation of transforming growth factor-β induced the EMT and also selectively retarded IFN-γ-responsive gene expression as well as IFN-γ-induced signal transducer and activator of transcription 1 activation, major histocompatibility complex I, and CD54 expression, cell migration/invasion inhibition, and direct/indirect cytotoxicity. Without changes in IFN-γ receptors, excessive oxidative activation of Src homology-2 containing phosphatase 2 (SHP2) in cells undergoing the EMT primarily caused cellular hyporesponsiveness to IFN-γ signaling and cytotoxicity, while combining an SHP2 inhibitor or antioxidant sensitized EMT-associated AS2 and mesenchymal A549 cells to IFN-γ-induced priming effects on tumor necrosis factor-related apoptosis-inducing ligand cytotoxicity. In cell line-derived xenograft models, combined treatment with IFN-γ and an SHP2 inhibitor induced enhanced anticancer activities. These results imply that EMT-associated SHP2 activation inhibits IFN-γ signaling, facilitating lung cancer cell escape from IFN-γ immunosurveillance.
•The malignant lung cancer cells acquire EMT to escape from IFN-γ immunosurveillance.•SHP2 in EMT cells determine cellular hyporesponsiveness to IFN-γ signaling and cytotoxicity.•Combined treatment with IFN-γ and an SHP2 inhibitor induced enhances anticancer therapy in vitro and in vivo.</abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>35490920</pmid><doi>10.1016/j.canlet.2022.215712</doi><tpages>1</tpages></addata></record> |
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| subjects | Adenocarcinoma Antioxidants Apoptosis Cell adhesion & migration Cell culture Cell Line, Tumor Cell migration Cell Movement - immunology Cytokines Cytotoxicity EMT Epithelial-Mesenchymal Transition - immunology Gene expression Genetic engineering Genomic analysis Growth factors Homology Humans Hypoxia IFN-γ Immunologic Surveillance Immunosurveillance Interferon-gamma - immunology Interferon-gamma - pharmacology Kinases Lung cancer Lung Neoplasms - drug therapy Lung Neoplasms - genetics Lung Neoplasms - immunology Lung Neoplasms - pathology Major histocompatibility complex Mesenchyme Metastases Metastasis MHC Migration inhibition Monoclonal antibodies Morphology Phosphatase Proteins Software STAT1 TRAIL protein Transcription activation Tumor necrosis factor-TNF Xenografts γ-Interferon |
| title | Epithelial-to-mesenchymal transition hinders interferon-γ-dependent immunosurveillance in lung cancer cells |
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