Activation of MAL2 by RAD21 inhibits the expression of MHC-I in immune evasion of endometrial cancer
CD8 + T cells are the primary mediators of anticancer immunity, and modulation of the CD8 + T cell response has been a central focus of immunotherapy to treat cancer. When CD8 + T cells specifically recognize antigenic peptides presented by the MHC-I on tumor cells, they become activated and kill th...
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| Veröffentlicht in: | Cytotechnology (Dordrecht) 2024-08, Vol.76 (4), p.465-482 |
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| container_title | Cytotechnology (Dordrecht) |
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| creator | Jin, Yuni Lu, Xiaoning Liu, Yuan Su, Liangdi Bao, Chan Guo, Huiming |
| description | CD8
+
T cells are the primary mediators of anticancer immunity, and modulation of the CD8
+
T cell response has been a central focus of immunotherapy to treat cancer. When CD8
+
T cells specifically recognize antigenic peptides presented by the MHC-I on tumor cells, they become activated and kill the tumor cells. However, one pivotal mechanism through which tumor cells evade immune surveillance is to reduce their antigen presentation. To identify novel immunotherapeutic targets, we specifically focused on the role of MAL2 in immune evasion in endometrial cancer (EC) and the underlying mechanism. MAL2 was overexpressed in EC tissues and cells and its transcription was enhanced by RAD21. Knockdown of MAL2 or RAD21 inhibited malignant behavior and immune evasion of EC cells by repressing MHC-I expression and the cytotoxic effects of CD8
+
cells. Conversely, MAL2 promoted immune evasion of EC cells and tumor growth in mice in the presence of RAD21 knockdown. These results indicate that RAD21 activation of MAL2 inhibits antigen processing and presentation of MHC-I, thereby inducing immune evasion of EC cells. We further suggest that RAD21 and MAL2 may serve as novel targets for EC immunotherapy. |
| doi_str_mv | 10.1007/s10616-024-00629-y |
| format | Article |
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+
T cells are the primary mediators of anticancer immunity, and modulation of the CD8
+
T cell response has been a central focus of immunotherapy to treat cancer. When CD8
+
T cells specifically recognize antigenic peptides presented by the MHC-I on tumor cells, they become activated and kill the tumor cells. However, one pivotal mechanism through which tumor cells evade immune surveillance is to reduce their antigen presentation. To identify novel immunotherapeutic targets, we specifically focused on the role of MAL2 in immune evasion in endometrial cancer (EC) and the underlying mechanism. MAL2 was overexpressed in EC tissues and cells and its transcription was enhanced by RAD21. Knockdown of MAL2 or RAD21 inhibited malignant behavior and immune evasion of EC cells by repressing MHC-I expression and the cytotoxic effects of CD8
+
cells. Conversely, MAL2 promoted immune evasion of EC cells and tumor growth in mice in the presence of RAD21 knockdown. These results indicate that RAD21 activation of MAL2 inhibits antigen processing and presentation of MHC-I, thereby inducing immune evasion of EC cells. We further suggest that RAD21 and MAL2 may serve as novel targets for EC immunotherapy.</description><identifier>ISSN: 0920-9069</identifier><identifier>EISSN: 1573-0778</identifier><identifier>DOI: 10.1007/s10616-024-00629-y</identifier><identifier>PMID: 38933871</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Antigen presentation ; Antigen processing ; Antigens ; Biochemistry ; Biomedicine ; Biotechnology ; Cancer therapies ; CD8 antigen ; Cells ; Chemistry ; Chemistry and Materials Science ; Cytotoxicity ; Dehydrogenases ; Endometrial cancer ; Endometrium ; Immune evasion ; Immunosurveillance ; Immunotherapy ; Lymphocytes ; Lymphocytes T ; Major histocompatibility complex ; Medical prognosis ; Pancreatic cancer ; Proteins ; Reagents ; Tumor cells ; Tumors ; Uterine cancer</subject><ispartof>Cytotechnology (Dordrecht), 2024-08, Vol.76 (4), p.465-482</ispartof><rights>The Author(s), under exclusive licence to Springer Nature B.V. 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><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c326t-ccc8875beda5bcd776088136751a88fa66974ab29937890588cb9474ef7085983</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10616-024-00629-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10616-024-00629-y$$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/38933871$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jin, Yuni</creatorcontrib><creatorcontrib>Lu, Xiaoning</creatorcontrib><creatorcontrib>Liu, Yuan</creatorcontrib><creatorcontrib>Su, Liangdi</creatorcontrib><creatorcontrib>Bao, Chan</creatorcontrib><creatorcontrib>Guo, Huiming</creatorcontrib><title>Activation of MAL2 by RAD21 inhibits the expression of MHC-I in immune evasion of endometrial cancer</title><title>Cytotechnology (Dordrecht)</title><addtitle>Cytotechnology</addtitle><addtitle>Cytotechnology</addtitle><description>CD8
+
T cells are the primary mediators of anticancer immunity, and modulation of the CD8
+
T cell response has been a central focus of immunotherapy to treat cancer. When CD8
+
T cells specifically recognize antigenic peptides presented by the MHC-I on tumor cells, they become activated and kill the tumor cells. However, one pivotal mechanism through which tumor cells evade immune surveillance is to reduce their antigen presentation. To identify novel immunotherapeutic targets, we specifically focused on the role of MAL2 in immune evasion in endometrial cancer (EC) and the underlying mechanism. MAL2 was overexpressed in EC tissues and cells and its transcription was enhanced by RAD21. Knockdown of MAL2 or RAD21 inhibited malignant behavior and immune evasion of EC cells by repressing MHC-I expression and the cytotoxic effects of CD8
+
cells. Conversely, MAL2 promoted immune evasion of EC cells and tumor growth in mice in the presence of RAD21 knockdown. These results indicate that RAD21 activation of MAL2 inhibits antigen processing and presentation of MHC-I, thereby inducing immune evasion of EC cells. We further suggest that RAD21 and MAL2 may serve as novel targets for EC immunotherapy.</description><subject>Antigen presentation</subject><subject>Antigen processing</subject><subject>Antigens</subject><subject>Biochemistry</subject><subject>Biomedicine</subject><subject>Biotechnology</subject><subject>Cancer therapies</subject><subject>CD8 antigen</subject><subject>Cells</subject><subject>Chemistry</subject><subject>Chemistry and Materials Science</subject><subject>Cytotoxicity</subject><subject>Dehydrogenases</subject><subject>Endometrial cancer</subject><subject>Endometrium</subject><subject>Immune evasion</subject><subject>Immunosurveillance</subject><subject>Immunotherapy</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Major histocompatibility complex</subject><subject>Medical prognosis</subject><subject>Pancreatic cancer</subject><subject>Proteins</subject><subject>Reagents</subject><subject>Tumor cells</subject><subject>Tumors</subject><subject>Uterine cancer</subject><issn>0920-9069</issn><issn>1573-0778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp9kUtP3DAUha2Kqgy0f6CLyhIbNoZrO_FjORoegzSoEqJry3GcYjRJpnYyIv8ewzBUYsHqLs53zr26B6GfFM4ogDxPFAQVBFhBAATTZPqCZrSUnICU6gDNQDMgGoQ-REcpPQKAlpR_Q4dcac6VpDNUz90QtnYIfYf7Bt_OVwxXE76bXzCKQ_cQqjAkPDx47J820ae0B5cLcpMBHNp27LK6tXvJd3Xf-iEGu8bOds7H7-hrY9fJ_3ibx-jP1eX9YklWv69vFvMVcZyJgTjnlJJl5WtbVq6WUoBSlAtZUqtUY4XQsrAV05pLpaFUylW6kIVvJKhSK36MTne5m9j_G30aTBuS8-u17Xw_JsNBMkWLgomMnnxAH_sxdvm6F4oKDkIWmWI7ysU-pegbs4mhtXEyFMxLB2bXgckdmNcOzJRNv96ix6r19btl__QM8B2QstT99fH_7k9inwHclo-J</recordid><startdate>20240801</startdate><enddate>20240801</enddate><creator>Jin, Yuni</creator><creator>Lu, Xiaoning</creator><creator>Liu, Yuan</creator><creator>Su, Liangdi</creator><creator>Bao, Chan</creator><creator>Guo, Huiming</creator><general>Springer Netherlands</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20240801</creationdate><title>Activation of MAL2 by RAD21 inhibits the expression of MHC-I in immune evasion of endometrial cancer</title><author>Jin, Yuni ; Lu, Xiaoning ; Liu, Yuan ; Su, Liangdi ; Bao, Chan ; Guo, Huiming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c326t-ccc8875beda5bcd776088136751a88fa66974ab29937890588cb9474ef7085983</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Antigen presentation</topic><topic>Antigen processing</topic><topic>Antigens</topic><topic>Biochemistry</topic><topic>Biomedicine</topic><topic>Biotechnology</topic><topic>Cancer therapies</topic><topic>CD8 antigen</topic><topic>Cells</topic><topic>Chemistry</topic><topic>Chemistry and Materials Science</topic><topic>Cytotoxicity</topic><topic>Dehydrogenases</topic><topic>Endometrial cancer</topic><topic>Endometrium</topic><topic>Immune evasion</topic><topic>Immunosurveillance</topic><topic>Immunotherapy</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Major histocompatibility complex</topic><topic>Medical prognosis</topic><topic>Pancreatic cancer</topic><topic>Proteins</topic><topic>Reagents</topic><topic>Tumor cells</topic><topic>Tumors</topic><topic>Uterine cancer</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jin, Yuni</creatorcontrib><creatorcontrib>Lu, Xiaoning</creatorcontrib><creatorcontrib>Liu, Yuan</creatorcontrib><creatorcontrib>Su, Liangdi</creatorcontrib><creatorcontrib>Bao, Chan</creatorcontrib><creatorcontrib>Guo, Huiming</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Cytotechnology (Dordrecht)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jin, Yuni</au><au>Lu, Xiaoning</au><au>Liu, Yuan</au><au>Su, Liangdi</au><au>Bao, Chan</au><au>Guo, Huiming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of MAL2 by RAD21 inhibits the expression of MHC-I in immune evasion of endometrial cancer</atitle><jtitle>Cytotechnology (Dordrecht)</jtitle><stitle>Cytotechnology</stitle><addtitle>Cytotechnology</addtitle><date>2024-08-01</date><risdate>2024</risdate><volume>76</volume><issue>4</issue><spage>465</spage><epage>482</epage><pages>465-482</pages><issn>0920-9069</issn><eissn>1573-0778</eissn><abstract>CD8
+
T cells are the primary mediators of anticancer immunity, and modulation of the CD8
+
T cell response has been a central focus of immunotherapy to treat cancer. When CD8
+
T cells specifically recognize antigenic peptides presented by the MHC-I on tumor cells, they become activated and kill the tumor cells. However, one pivotal mechanism through which tumor cells evade immune surveillance is to reduce their antigen presentation. To identify novel immunotherapeutic targets, we specifically focused on the role of MAL2 in immune evasion in endometrial cancer (EC) and the underlying mechanism. MAL2 was overexpressed in EC tissues and cells and its transcription was enhanced by RAD21. Knockdown of MAL2 or RAD21 inhibited malignant behavior and immune evasion of EC cells by repressing MHC-I expression and the cytotoxic effects of CD8
+
cells. Conversely, MAL2 promoted immune evasion of EC cells and tumor growth in mice in the presence of RAD21 knockdown. These results indicate that RAD21 activation of MAL2 inhibits antigen processing and presentation of MHC-I, thereby inducing immune evasion of EC cells. We further suggest that RAD21 and MAL2 may serve as novel targets for EC immunotherapy.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>38933871</pmid><doi>10.1007/s10616-024-00629-y</doi><tpages>18</tpages></addata></record> |
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| subjects | Antigen presentation Antigen processing Antigens Biochemistry Biomedicine Biotechnology Cancer therapies CD8 antigen Cells Chemistry Chemistry and Materials Science Cytotoxicity Dehydrogenases Endometrial cancer Endometrium Immune evasion Immunosurveillance Immunotherapy Lymphocytes Lymphocytes T Major histocompatibility complex Medical prognosis Pancreatic cancer Proteins Reagents Tumor cells Tumors Uterine cancer |
| title | Activation of MAL2 by RAD21 inhibits the expression of MHC-I in immune evasion of endometrial cancer |
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