Death receptors 4/5 mediate tumour sensitivity to natural killer cell-mediated cytotoxicity in mismatch repair deficient colorectal cancer
Background Identifying the target of natural killer (NK) cells in colorectal cancer (CRC) is critical for optimising the clinical use of NK cell-mediated immunotherapy. Mismatch repair deficiency (dMMR) is associated with high immune cell infiltration and MHC Class I defects. Whether dMMR CRC respon...
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| Veröffentlicht in: | British journal of cancer 2024-07, Vol.131 (2), p.334-346 |
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| creator | Yang, Lin Yi, Jiahong He, Wenzhuo Kong, Pengfei Xie, Qiankun Jin, Yanan Xiong, Zhenchong Xia, Liangping |
| description | Background
Identifying the target of natural killer (NK) cells in colorectal cancer (CRC) is critical for optimising the clinical use of NK cell-mediated immunotherapy. Mismatch repair deficiency (dMMR) is associated with high immune cell infiltration and MHC Class I defects. Whether dMMR CRC responses to NK cell therapy remains unclear.
Methods
MLH1, DR4, and DR5 knockout cell lines were established using CRISPR-Cas9 system. NK92-MI or NK cell isolated from BABL/C mice were used as effector cells against tumour cells. Inflammatory cytokines secretion by CRC cells was assessed via cytokine analysis. NK-cell-deficient/proficient animal models were used to validate the NK cell sensitivity.
Results
We observed that dMMR CRC cells were more sensitive to NK cell-mediated cytotoxicity than were mismatch-repair-proficient (pMMR) CRC cells. In dMMR CRC, Death receptor (DR)4/5 was upregulated and mediated sensitivity to NK cell-mediated cytotoxicity. DR4/5-mediated secretion of interleukin -12 sustained NK cell viability in dMMR CRC. NK cell depletion induced dMMR CRC tumour growth, and NK cell transfer inhibited lung metastasis of dMMR CRC with DR4/5 expression in vivo. TP53 upregulated DR4/DR5 expression in dMMR CRC.
Conclusions
dMMR associated with increased sensitivity to NK cell-mediated cytotoxicity in CRC. DR4/DR5 sensitise dMMR CRC to NK cell-mediated cytotoxicity. |
| doi_str_mv | 10.1038/s41416-024-02673-z |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_pubmed_primary_38796599</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3060747618</sourcerecordid><originalsourceid>FETCH-LOGICAL-c171z-b242c628ac12a069509c53c5d250482eec124dbf39738b2af7a39cb6866666843</originalsourceid><addsrcrecordid>eNp9kU2PFCEQhonRuOPqH_BgSLx4aZevBvpo1s9kEy96JjRdrazdzQi0ceYn-KutdkZNPEhSIVBPvVXwEvKYs-ecSXtVFFdcN0woDG1kc7xDdryVouFWmLtkxxgzDesEuyAPSrnFY8esuU8upDWdbrtuR368BF8_0wwB9jXlQtVVS2cYoq9A6zqnNdMCS4k1fov1QGuii69r9hP9EqcJMg0wTc25YqDhUFNN32PY4LjQOZbZ17B12PuY6QAj5mCpNKQpYduKSsEvAfJDcm_0U4FH5_2SfHz96sP12-bm_Zt31y9umsANPza9UCJoYX3gwjPdtawLrQztIFqmrADAezX0o-yMtL3wo_GyC722eltWyUvy7KS7z-nrCqU6HHJ7hV8grcVJpplRRnOL6NN_0Fv8kAWnQ8pKDK0FUuJEhZxKyTC6fY6zzwfHmduccienHDrlfjnljlj05Cy99vh7f0p-W4OAPAEFU8snyH97_0f2JyDToN8</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>3083308662</pqid></control><display><type>article</type><title>Death receptors 4/5 mediate tumour sensitivity to natural killer cell-mediated cytotoxicity in mismatch repair deficient colorectal cancer</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Yang, Lin ; Yi, Jiahong ; He, Wenzhuo ; Kong, Pengfei ; Xie, Qiankun ; Jin, Yanan ; Xiong, Zhenchong ; Xia, Liangping</creator><creatorcontrib>Yang, Lin ; Yi, Jiahong ; He, Wenzhuo ; Kong, Pengfei ; Xie, Qiankun ; Jin, Yanan ; Xiong, Zhenchong ; Xia, Liangping</creatorcontrib><description>Background
Identifying the target of natural killer (NK) cells in colorectal cancer (CRC) is critical for optimising the clinical use of NK cell-mediated immunotherapy. Mismatch repair deficiency (dMMR) is associated with high immune cell infiltration and MHC Class I defects. Whether dMMR CRC responses to NK cell therapy remains unclear.
Methods
MLH1, DR4, and DR5 knockout cell lines were established using CRISPR-Cas9 system. NK92-MI or NK cell isolated from BABL/C mice were used as effector cells against tumour cells. Inflammatory cytokines secretion by CRC cells was assessed via cytokine analysis. NK-cell-deficient/proficient animal models were used to validate the NK cell sensitivity.
Results
We observed that dMMR CRC cells were more sensitive to NK cell-mediated cytotoxicity than were mismatch-repair-proficient (pMMR) CRC cells. In dMMR CRC, Death receptor (DR)4/5 was upregulated and mediated sensitivity to NK cell-mediated cytotoxicity. DR4/5-mediated secretion of interleukin -12 sustained NK cell viability in dMMR CRC. NK cell depletion induced dMMR CRC tumour growth, and NK cell transfer inhibited lung metastasis of dMMR CRC with DR4/5 expression in vivo. TP53 upregulated DR4/DR5 expression in dMMR CRC.
Conclusions
dMMR associated with increased sensitivity to NK cell-mediated cytotoxicity in CRC. DR4/DR5 sensitise dMMR CRC to NK cell-mediated cytotoxicity.</description><identifier>ISSN: 0007-0920</identifier><identifier>ISSN: 1532-1827</identifier><identifier>EISSN: 1532-1827</identifier><identifier>DOI: 10.1038/s41416-024-02673-z</identifier><identifier>PMID: 38796599</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>692/499 ; 692/53/2422 ; Animal models ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Brain Neoplasms ; Cancer Research ; Cell culture ; Cell death ; Cell Line, Tumor ; Cell therapy ; Cell viability ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - immunology ; Colorectal Neoplasms - pathology ; CRISPR ; Cytotoxicity ; Cytotoxicity, Immunologic ; Death receptors ; DNA Mismatch Repair ; Drug Resistance ; Effector cells ; Epidemiology ; Humans ; Immunotherapy ; Killer Cells, Natural - immunology ; Killer Cells, Natural - metabolism ; Major histocompatibility complex ; Metastases ; Mice ; Mice, Inbred BALB C ; Mismatch repair ; MLH1 protein ; Molecular Medicine ; MutL Protein Homolog 1 - deficiency ; MutL Protein Homolog 1 - genetics ; MutL Protein Homolog 1 - metabolism ; Natural killer cells ; Neoplastic Syndromes, Hereditary - genetics ; Neoplastic Syndromes, Hereditary - immunology ; Neoplastic Syndromes, Hereditary - pathology ; Oncology ; Receptors, TNF-Related Apoptosis-Inducing Ligand - genetics ; Receptors, TNF-Related Apoptosis-Inducing Ligand - metabolism ; Tumors</subject><ispartof>British journal of cancer, 2024-07, Vol.131 (2), p.334-346</ispartof><rights>The Author(s), under exclusive licence to Springer Nature Limited 2024. corrected publication 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2024. The Author(s), under exclusive licence to Springer Nature Limited.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c171z-b242c628ac12a069509c53c5d250482eec124dbf39738b2af7a39cb6866666843</cites><orcidid>0000-0003-4544-8071 ; 0000-0001-7532-4913 ; 0000-0002-1129-5663</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/s41416-024-02673-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/s41416-024-02673-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51298</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38796599$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Lin</creatorcontrib><creatorcontrib>Yi, Jiahong</creatorcontrib><creatorcontrib>He, Wenzhuo</creatorcontrib><creatorcontrib>Kong, Pengfei</creatorcontrib><creatorcontrib>Xie, Qiankun</creatorcontrib><creatorcontrib>Jin, Yanan</creatorcontrib><creatorcontrib>Xiong, Zhenchong</creatorcontrib><creatorcontrib>Xia, Liangping</creatorcontrib><title>Death receptors 4/5 mediate tumour sensitivity to natural killer cell-mediated cytotoxicity in mismatch repair deficient colorectal cancer</title><title>British journal of cancer</title><addtitle>Br J Cancer</addtitle><addtitle>Br J Cancer</addtitle><description>Background
Identifying the target of natural killer (NK) cells in colorectal cancer (CRC) is critical for optimising the clinical use of NK cell-mediated immunotherapy. Mismatch repair deficiency (dMMR) is associated with high immune cell infiltration and MHC Class I defects. Whether dMMR CRC responses to NK cell therapy remains unclear.
Methods
MLH1, DR4, and DR5 knockout cell lines were established using CRISPR-Cas9 system. NK92-MI or NK cell isolated from BABL/C mice were used as effector cells against tumour cells. Inflammatory cytokines secretion by CRC cells was assessed via cytokine analysis. NK-cell-deficient/proficient animal models were used to validate the NK cell sensitivity.
Results
We observed that dMMR CRC cells were more sensitive to NK cell-mediated cytotoxicity than were mismatch-repair-proficient (pMMR) CRC cells. In dMMR CRC, Death receptor (DR)4/5 was upregulated and mediated sensitivity to NK cell-mediated cytotoxicity. DR4/5-mediated secretion of interleukin -12 sustained NK cell viability in dMMR CRC. NK cell depletion induced dMMR CRC tumour growth, and NK cell transfer inhibited lung metastasis of dMMR CRC with DR4/5 expression in vivo. TP53 upregulated DR4/DR5 expression in dMMR CRC.
Conclusions
dMMR associated with increased sensitivity to NK cell-mediated cytotoxicity in CRC. DR4/DR5 sensitise dMMR CRC to NK cell-mediated cytotoxicity.</description><subject>692/499</subject><subject>692/53/2422</subject><subject>Animal models</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain Neoplasms</subject><subject>Cancer Research</subject><subject>Cell culture</subject><subject>Cell death</subject><subject>Cell Line, Tumor</subject><subject>Cell therapy</subject><subject>Cell viability</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - immunology</subject><subject>Colorectal Neoplasms - pathology</subject><subject>CRISPR</subject><subject>Cytotoxicity</subject><subject>Cytotoxicity, Immunologic</subject><subject>Death receptors</subject><subject>DNA Mismatch Repair</subject><subject>Drug Resistance</subject><subject>Effector cells</subject><subject>Epidemiology</subject><subject>Humans</subject><subject>Immunotherapy</subject><subject>Killer Cells, Natural - immunology</subject><subject>Killer Cells, Natural - metabolism</subject><subject>Major histocompatibility complex</subject><subject>Metastases</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mismatch repair</subject><subject>MLH1 protein</subject><subject>Molecular Medicine</subject><subject>MutL Protein Homolog 1 - deficiency</subject><subject>MutL Protein Homolog 1 - genetics</subject><subject>MutL Protein Homolog 1 - metabolism</subject><subject>Natural killer cells</subject><subject>Neoplastic Syndromes, Hereditary - genetics</subject><subject>Neoplastic Syndromes, Hereditary - immunology</subject><subject>Neoplastic Syndromes, Hereditary - pathology</subject><subject>Oncology</subject><subject>Receptors, TNF-Related Apoptosis-Inducing Ligand - genetics</subject><subject>Receptors, TNF-Related Apoptosis-Inducing Ligand - metabolism</subject><subject>Tumors</subject><issn>0007-0920</issn><issn>1532-1827</issn><issn>1532-1827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU2PFCEQhonRuOPqH_BgSLx4aZevBvpo1s9kEy96JjRdrazdzQi0ceYn-KutdkZNPEhSIVBPvVXwEvKYs-ecSXtVFFdcN0woDG1kc7xDdryVouFWmLtkxxgzDesEuyAPSrnFY8esuU8upDWdbrtuR368BF8_0wwB9jXlQtVVS2cYoq9A6zqnNdMCS4k1fov1QGuii69r9hP9EqcJMg0wTc25YqDhUFNN32PY4LjQOZbZ17B12PuY6QAj5mCpNKQpYduKSsEvAfJDcm_0U4FH5_2SfHz96sP12-bm_Zt31y9umsANPza9UCJoYX3gwjPdtawLrQztIFqmrADAezX0o-yMtL3wo_GyC722eltWyUvy7KS7z-nrCqU6HHJ7hV8grcVJpplRRnOL6NN_0Fv8kAWnQ8pKDK0FUuJEhZxKyTC6fY6zzwfHmduccienHDrlfjnljlj05Cy99vh7f0p-W4OAPAEFU8snyH97_0f2JyDToN8</recordid><startdate>202407</startdate><enddate>202407</enddate><creator>Yang, Lin</creator><creator>Yi, Jiahong</creator><creator>He, Wenzhuo</creator><creator>Kong, Pengfei</creator><creator>Xie, Qiankun</creator><creator>Jin, Yanan</creator><creator>Xiong, Zhenchong</creator><creator>Xia, Liangping</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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><orcidid>https://orcid.org/0000-0003-4544-8071</orcidid><orcidid>https://orcid.org/0000-0001-7532-4913</orcidid><orcidid>https://orcid.org/0000-0002-1129-5663</orcidid></search><sort><creationdate>202407</creationdate><title>Death receptors 4/5 mediate tumour sensitivity to natural killer cell-mediated cytotoxicity in mismatch repair deficient colorectal cancer</title><author>Yang, Lin ; Yi, Jiahong ; He, Wenzhuo ; Kong, Pengfei ; Xie, Qiankun ; Jin, Yanan ; Xiong, Zhenchong ; Xia, Liangping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c171z-b242c628ac12a069509c53c5d250482eec124dbf39738b2af7a39cb6866666843</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>692/499</topic><topic>692/53/2422</topic><topic>Animal models</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain Neoplasms</topic><topic>Cancer Research</topic><topic>Cell culture</topic><topic>Cell death</topic><topic>Cell Line, Tumor</topic><topic>Cell therapy</topic><topic>Cell viability</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - immunology</topic><topic>Colorectal Neoplasms - pathology</topic><topic>CRISPR</topic><topic>Cytotoxicity</topic><topic>Cytotoxicity, Immunologic</topic><topic>Death receptors</topic><topic>DNA Mismatch Repair</topic><topic>Drug Resistance</topic><topic>Effector cells</topic><topic>Epidemiology</topic><topic>Humans</topic><topic>Immunotherapy</topic><topic>Killer Cells, Natural - immunology</topic><topic>Killer Cells, Natural - metabolism</topic><topic>Major histocompatibility complex</topic><topic>Metastases</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mismatch repair</topic><topic>MLH1 protein</topic><topic>Molecular Medicine</topic><topic>MutL Protein Homolog 1 - deficiency</topic><topic>MutL Protein Homolog 1 - genetics</topic><topic>MutL Protein Homolog 1 - metabolism</topic><topic>Natural killer cells</topic><topic>Neoplastic Syndromes, Hereditary - genetics</topic><topic>Neoplastic Syndromes, Hereditary - immunology</topic><topic>Neoplastic Syndromes, Hereditary - pathology</topic><topic>Oncology</topic><topic>Receptors, TNF-Related Apoptosis-Inducing Ligand - genetics</topic><topic>Receptors, TNF-Related Apoptosis-Inducing Ligand - metabolism</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Lin</creatorcontrib><creatorcontrib>Yi, Jiahong</creatorcontrib><creatorcontrib>He, Wenzhuo</creatorcontrib><creatorcontrib>Kong, Pengfei</creatorcontrib><creatorcontrib>Xie, Qiankun</creatorcontrib><creatorcontrib>Jin, Yanan</creatorcontrib><creatorcontrib>Xiong, Zhenchong</creatorcontrib><creatorcontrib>Xia, Liangping</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>British journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Lin</au><au>Yi, Jiahong</au><au>He, Wenzhuo</au><au>Kong, Pengfei</au><au>Xie, Qiankun</au><au>Jin, Yanan</au><au>Xiong, Zhenchong</au><au>Xia, Liangping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Death receptors 4/5 mediate tumour sensitivity to natural killer cell-mediated cytotoxicity in mismatch repair deficient colorectal cancer</atitle><jtitle>British journal of cancer</jtitle><stitle>Br J Cancer</stitle><addtitle>Br J Cancer</addtitle><date>2024-07</date><risdate>2024</risdate><volume>131</volume><issue>2</issue><spage>334</spage><epage>346</epage><pages>334-346</pages><issn>0007-0920</issn><issn>1532-1827</issn><eissn>1532-1827</eissn><abstract>Background
Identifying the target of natural killer (NK) cells in colorectal cancer (CRC) is critical for optimising the clinical use of NK cell-mediated immunotherapy. Mismatch repair deficiency (dMMR) is associated with high immune cell infiltration and MHC Class I defects. Whether dMMR CRC responses to NK cell therapy remains unclear.
Methods
MLH1, DR4, and DR5 knockout cell lines were established using CRISPR-Cas9 system. NK92-MI or NK cell isolated from BABL/C mice were used as effector cells against tumour cells. Inflammatory cytokines secretion by CRC cells was assessed via cytokine analysis. NK-cell-deficient/proficient animal models were used to validate the NK cell sensitivity.
Results
We observed that dMMR CRC cells were more sensitive to NK cell-mediated cytotoxicity than were mismatch-repair-proficient (pMMR) CRC cells. In dMMR CRC, Death receptor (DR)4/5 was upregulated and mediated sensitivity to NK cell-mediated cytotoxicity. DR4/5-mediated secretion of interleukin -12 sustained NK cell viability in dMMR CRC. NK cell depletion induced dMMR CRC tumour growth, and NK cell transfer inhibited lung metastasis of dMMR CRC with DR4/5 expression in vivo. TP53 upregulated DR4/DR5 expression in dMMR CRC.
Conclusions
dMMR associated with increased sensitivity to NK cell-mediated cytotoxicity in CRC. DR4/DR5 sensitise dMMR CRC to NK cell-mediated cytotoxicity.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>38796599</pmid><doi>10.1038/s41416-024-02673-z</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0003-4544-8071</orcidid><orcidid>https://orcid.org/0000-0001-7532-4913</orcidid><orcidid>https://orcid.org/0000-0002-1129-5663</orcidid></addata></record> |
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| subjects | 692/499 692/53/2422 Animal models Animals Biomedical and Life Sciences Biomedicine Brain Neoplasms Cancer Research Cell culture Cell death Cell Line, Tumor Cell therapy Cell viability Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - genetics Colorectal Neoplasms - immunology Colorectal Neoplasms - pathology CRISPR Cytotoxicity Cytotoxicity, Immunologic Death receptors DNA Mismatch Repair Drug Resistance Effector cells Epidemiology Humans Immunotherapy Killer Cells, Natural - immunology Killer Cells, Natural - metabolism Major histocompatibility complex Metastases Mice Mice, Inbred BALB C Mismatch repair MLH1 protein Molecular Medicine MutL Protein Homolog 1 - deficiency MutL Protein Homolog 1 - genetics MutL Protein Homolog 1 - metabolism Natural killer cells Neoplastic Syndromes, Hereditary - genetics Neoplastic Syndromes, Hereditary - immunology Neoplastic Syndromes, Hereditary - pathology Oncology Receptors, TNF-Related Apoptosis-Inducing Ligand - genetics Receptors, TNF-Related Apoptosis-Inducing Ligand - metabolism Tumors |
| title | Death receptors 4/5 mediate tumour sensitivity to natural killer cell-mediated cytotoxicity in mismatch repair deficient colorectal cancer |
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