Interleukin‐17 is associated with expression of programmed cell death 1 ligand 1 in ovarian carcinoma
The programmed cell death 1/programmed cell death 1 ligand 1 pathway was successfully targeted in cancer immunotherapy. Elevated interleukin‐17 (IL‐17), which is known in autoimmune diseases, has recently been recognized in cancer patients. We investigated the role of IL‐17 in the regulation of expr...
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| Veröffentlicht in: | Cancer science 2019-10, Vol.110 (10), p.3068-3078 |
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| creator | Aotsuka, Aeri Matsumoto, Yoko Arimoto, Takahide Kawata, Akira Ogishima, Juri Taguchi, Ayumi Tanikawa, Michihiro Sone, Kenbun Mori‐Uchino, Mayuyo Tsuruga, Tetsushi Oda, Katsutoshi Kawana, Kei Osuga, Yutaka Fujii, Tomoyuki |
| description | The programmed cell death 1/programmed cell death 1 ligand 1 pathway was successfully targeted in cancer immunotherapy. Elevated interleukin‐17 (IL‐17), which is known in autoimmune diseases, has recently been recognized in cancer patients. We investigated the role of IL‐17 in the regulation of expression of programmed cell death 1 ligand 1 in ovarian cancer by evaluating changes in the number of IL‐17‐producing cluster of differentiation 4 helper T cells (Th17) and γδT cells (γδT17) in PBMC of 52 gynecological cancer patients (including 30 ovarian cancer patients) and 18 healthy controls. The occupancy ratio of Th17 and γδT17 was higher in ovarian cancer and endometrial cancer patients than in controls, determined by multi‐color flow cytometry (Th17: P |
| doi_str_mv | 10.1111/cas.14174 |
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Although the relationship between IL‐17 and PD‐L1 in ovarian cancer (OC) is not well understood, we found that IL‐17 positively modulates the expression of PD‐L1 and associated factors, IL‐6 and pSTAT3. The number of IL‐17‐producing CD4+ helper T cells (Th17) was positively correlated with the neutrophil‐to‐lymphocyte ratio, which is a prognostic biomarker in OC. Thus, elevated Th17 count and IL‐17 level may predict PD‐L1 overexpression and poor prognosis in OC.</description><identifier>ISSN: 1347-9032</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/cas.14174</identifier><identifier>PMID: 31432577</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Adult ; Aged ; Antigens ; Apoptosis ; Autoimmune diseases ; B7-H1 Antigen - genetics ; Biomarkers ; Biotechnology ; Cancer immunotherapy ; Case-Control Studies ; Cell death ; Cell differentiation ; Cell Line, Tumor ; Cervical cancer ; Chemotherapy ; Cloning ; Cytokines ; Endometrial cancer ; Endometrial Neoplasms - genetics ; Endometrial Neoplasms - immunology ; Endometrium ; Feedback ; Female ; Flow cytometry ; Gene Expression Regulation, Neoplastic ; Growth factors ; Gynecology ; Helper cells ; Humans ; IL‐17 ; Immunotherapy ; Infections ; Interleukin-16 - metabolism ; Interleukin-17 - genetics ; Interleukin-17 - metabolism ; Intraepithelial Lymphocytes - metabolism ; Ligands ; Lymphocytes ; Lymphocytes T ; Medical prognosis ; neutrophil‐to‐lymphocyte ratio ; Original ; Ovarian cancer ; Ovarian carcinoma ; Ovarian Neoplasms - genetics ; Ovarian Neoplasms - immunology ; Patients ; PD-1 protein ; PD‐L1 ; Penicillin ; Peripheral blood mononuclear cells ; Phosphorylation ; Plasma ; Prognosis ; Signal transduction ; STAT3 Transcription Factor - metabolism ; T cell receptors ; Th17 ; Th17 Cells - metabolism ; Transcription ; Tumor necrosis factor-TNF ; Tumors ; Up-Regulation</subject><ispartof>Cancer science, 2019-10, Vol.110 (10), p.3068-3078</ispartof><rights>2019 The Authors. published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2019 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2019. This work is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4954-582ee37b5e7101ffc67ec8a26fe085eecb598a3969976fea78b094632c3f8b7b3</citedby><cites>FETCH-LOGICAL-c4954-582ee37b5e7101ffc67ec8a26fe085eecb598a3969976fea78b094632c3f8b7b3</cites><orcidid>0000-0001-9242-0069</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6778630/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6778630/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31432577$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aotsuka, Aeri</creatorcontrib><creatorcontrib>Matsumoto, Yoko</creatorcontrib><creatorcontrib>Arimoto, Takahide</creatorcontrib><creatorcontrib>Kawata, Akira</creatorcontrib><creatorcontrib>Ogishima, Juri</creatorcontrib><creatorcontrib>Taguchi, Ayumi</creatorcontrib><creatorcontrib>Tanikawa, Michihiro</creatorcontrib><creatorcontrib>Sone, Kenbun</creatorcontrib><creatorcontrib>Mori‐Uchino, Mayuyo</creatorcontrib><creatorcontrib>Tsuruga, Tetsushi</creatorcontrib><creatorcontrib>Oda, Katsutoshi</creatorcontrib><creatorcontrib>Kawana, Kei</creatorcontrib><creatorcontrib>Osuga, Yutaka</creatorcontrib><creatorcontrib>Fujii, Tomoyuki</creatorcontrib><title>Interleukin‐17 is associated with expression of programmed cell death 1 ligand 1 in ovarian carcinoma</title><title>Cancer science</title><addtitle>Cancer Sci</addtitle><description>The programmed cell death 1/programmed cell death 1 ligand 1 pathway was successfully targeted in cancer immunotherapy. Elevated interleukin‐17 (IL‐17), which is known in autoimmune diseases, has recently been recognized in cancer patients. We investigated the role of IL‐17 in the regulation of expression of programmed cell death 1 ligand 1 in ovarian cancer by evaluating changes in the number of IL‐17‐producing cluster of differentiation 4 helper T cells (Th17) and γδT cells (γδT17) in PBMC of 52 gynecological cancer patients (including 30 ovarian cancer patients) and 18 healthy controls. The occupancy ratio of Th17 and γδT17 was higher in ovarian cancer and endometrial cancer patients than in controls, determined by multi‐color flow cytometry (Th17: P < 0.0001 and P = 0.0002, respectively; γδT17: P = 0.0020 and P = 0.0084, respectively). IL‐17 mRNA level was elevated in PBMC of ovarian cancer patients (P = 0.0029), as measured by RT‐PCR. The neutrophil‐to‐lymphocyte ratio, which is a prognostic biomarker of ovarian cancer, correlated with Th17 occupancy ratio in patients (P = 0.0068). We found that programmed cell death 1 ligand 1 expression and its associated factors (IL‐6 and phospho‐signal transducer and activator of transcription 3) were induced by IL‐17 in an ovarian cancer cell line. These results suggest that increased Th17 counts and IL‐17 level, which correlated with high neutrophil‐to‐lymphocyte ratio and programmed cell death 1 ligand 1 expression, are potential biomarkers for poor prognosis in ovarian cancer and likely indications for application of programmed cell death 1 ligand 1 pathway inhibitors.
Although the relationship between IL‐17 and PD‐L1 in ovarian cancer (OC) is not well understood, we found that IL‐17 positively modulates the expression of PD‐L1 and associated factors, IL‐6 and pSTAT3. The number of IL‐17‐producing CD4+ helper T cells (Th17) was positively correlated with the neutrophil‐to‐lymphocyte ratio, which is a prognostic biomarker in OC. Thus, elevated Th17 count and IL‐17 level may predict PD‐L1 overexpression and poor prognosis in OC.</description><subject>Adult</subject><subject>Aged</subject><subject>Antigens</subject><subject>Apoptosis</subject><subject>Autoimmune diseases</subject><subject>B7-H1 Antigen - genetics</subject><subject>Biomarkers</subject><subject>Biotechnology</subject><subject>Cancer immunotherapy</subject><subject>Case-Control Studies</subject><subject>Cell death</subject><subject>Cell differentiation</subject><subject>Cell Line, Tumor</subject><subject>Cervical cancer</subject><subject>Chemotherapy</subject><subject>Cloning</subject><subject>Cytokines</subject><subject>Endometrial cancer</subject><subject>Endometrial Neoplasms - genetics</subject><subject>Endometrial Neoplasms - immunology</subject><subject>Endometrium</subject><subject>Feedback</subject><subject>Female</subject><subject>Flow cytometry</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Growth factors</subject><subject>Gynecology</subject><subject>Helper cells</subject><subject>Humans</subject><subject>IL‐17</subject><subject>Immunotherapy</subject><subject>Infections</subject><subject>Interleukin-16 - metabolism</subject><subject>Interleukin-17 - genetics</subject><subject>Interleukin-17 - metabolism</subject><subject>Intraepithelial Lymphocytes - metabolism</subject><subject>Ligands</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Medical prognosis</subject><subject>neutrophil‐to‐lymphocyte ratio</subject><subject>Original</subject><subject>Ovarian cancer</subject><subject>Ovarian carcinoma</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Ovarian Neoplasms - immunology</subject><subject>Patients</subject><subject>PD-1 protein</subject><subject>PD‐L1</subject><subject>Penicillin</subject><subject>Peripheral blood mononuclear cells</subject><subject>Phosphorylation</subject><subject>Plasma</subject><subject>Prognosis</subject><subject>Signal transduction</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>T cell receptors</subject><subject>Th17</subject><subject>Th17 Cells - metabolism</subject><subject>Transcription</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumors</subject><subject>Up-Regulation</subject><issn>1347-9032</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kc9qFTEUxoMotlYXvoAE3Ohi2vybZLIRysU_hYILdR3O5J65TZ1JrslMa3c-gs_ok5j21qKCZpPDOT8-vo-PkKecHfL6jjyUQ664UffIPpfKNoYxff9mNo1lUuyRR6WcMya1suoh2ZNcSdEas082J3HGPOLyOcQf375zQ0OhUEryAWZc08swn1H8us1YSkiRpoFuc9pkmKZ69TiOdI1QGU7HsIG4rkOo2AXkAJF6yD7ENMFj8mCAseCT2_-AfHrz-uPqXXP6_u3J6vi08cq2qmk7gShN36LhjA-D1wZ9B0IPyLoW0fet7UBaba2pOzBdz6zSUng5dL3p5QF5tdPdLn116DHOGUa3zWGCfOUSBPfnJYYzt0kXThvTacmqwItbgZy-LFhmN4VynRMipqU4IazWWindVvT5X-h5WnKs8ZxQ2ohqVbP_UpJx1jLGeKVe7iifUykZhzvLnLnrkl0t2d2UXNlnv2e8I3-1WoGjHXAZRrz6t5JbHX_YSf4Ei3yxdg</recordid><startdate>201910</startdate><enddate>201910</enddate><creator>Aotsuka, Aeri</creator><creator>Matsumoto, Yoko</creator><creator>Arimoto, Takahide</creator><creator>Kawata, Akira</creator><creator>Ogishima, Juri</creator><creator>Taguchi, Ayumi</creator><creator>Tanikawa, Michihiro</creator><creator>Sone, Kenbun</creator><creator>Mori‐Uchino, Mayuyo</creator><creator>Tsuruga, Tetsushi</creator><creator>Oda, Katsutoshi</creator><creator>Kawana, Kei</creator><creator>Osuga, Yutaka</creator><creator>Fujii, Tomoyuki</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><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>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-9242-0069</orcidid></search><sort><creationdate>201910</creationdate><title>Interleukin‐17 is associated with expression of programmed cell death 1 ligand 1 in ovarian carcinoma</title><author>Aotsuka, Aeri ; Matsumoto, Yoko ; Arimoto, Takahide ; Kawata, Akira ; Ogishima, Juri ; Taguchi, Ayumi ; Tanikawa, Michihiro ; Sone, Kenbun ; Mori‐Uchino, Mayuyo ; Tsuruga, Tetsushi ; Oda, Katsutoshi ; Kawana, Kei ; Osuga, Yutaka ; Fujii, Tomoyuki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4954-582ee37b5e7101ffc67ec8a26fe085eecb598a3969976fea78b094632c3f8b7b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Antigens</topic><topic>Apoptosis</topic><topic>Autoimmune diseases</topic><topic>B7-H1 Antigen - genetics</topic><topic>Biomarkers</topic><topic>Biotechnology</topic><topic>Cancer immunotherapy</topic><topic>Case-Control Studies</topic><topic>Cell death</topic><topic>Cell differentiation</topic><topic>Cell Line, Tumor</topic><topic>Cervical cancer</topic><topic>Chemotherapy</topic><topic>Cloning</topic><topic>Cytokines</topic><topic>Endometrial cancer</topic><topic>Endometrial Neoplasms - genetics</topic><topic>Endometrial Neoplasms - immunology</topic><topic>Endometrium</topic><topic>Feedback</topic><topic>Female</topic><topic>Flow cytometry</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Growth factors</topic><topic>Gynecology</topic><topic>Helper cells</topic><topic>Humans</topic><topic>IL‐17</topic><topic>Immunotherapy</topic><topic>Infections</topic><topic>Interleukin-16 - metabolism</topic><topic>Interleukin-17 - genetics</topic><topic>Interleukin-17 - metabolism</topic><topic>Intraepithelial Lymphocytes - metabolism</topic><topic>Ligands</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Medical prognosis</topic><topic>neutrophil‐to‐lymphocyte ratio</topic><topic>Original</topic><topic>Ovarian cancer</topic><topic>Ovarian carcinoma</topic><topic>Ovarian Neoplasms - genetics</topic><topic>Ovarian Neoplasms - immunology</topic><topic>Patients</topic><topic>PD-1 protein</topic><topic>PD‐L1</topic><topic>Penicillin</topic><topic>Peripheral blood mononuclear cells</topic><topic>Phosphorylation</topic><topic>Plasma</topic><topic>Prognosis</topic><topic>Signal transduction</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>T cell receptors</topic><topic>Th17</topic><topic>Th17 Cells - metabolism</topic><topic>Transcription</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumors</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aotsuka, Aeri</creatorcontrib><creatorcontrib>Matsumoto, Yoko</creatorcontrib><creatorcontrib>Arimoto, Takahide</creatorcontrib><creatorcontrib>Kawata, Akira</creatorcontrib><creatorcontrib>Ogishima, Juri</creatorcontrib><creatorcontrib>Taguchi, Ayumi</creatorcontrib><creatorcontrib>Tanikawa, Michihiro</creatorcontrib><creatorcontrib>Sone, Kenbun</creatorcontrib><creatorcontrib>Mori‐Uchino, Mayuyo</creatorcontrib><creatorcontrib>Tsuruga, Tetsushi</creatorcontrib><creatorcontrib>Oda, Katsutoshi</creatorcontrib><creatorcontrib>Kawana, Kei</creatorcontrib><creatorcontrib>Osuga, Yutaka</creatorcontrib><creatorcontrib>Fujii, Tomoyuki</creatorcontrib><collection>Wiley-Blackwell Open Access Titles</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aotsuka, Aeri</au><au>Matsumoto, Yoko</au><au>Arimoto, Takahide</au><au>Kawata, Akira</au><au>Ogishima, Juri</au><au>Taguchi, Ayumi</au><au>Tanikawa, Michihiro</au><au>Sone, Kenbun</au><au>Mori‐Uchino, Mayuyo</au><au>Tsuruga, Tetsushi</au><au>Oda, Katsutoshi</au><au>Kawana, Kei</au><au>Osuga, Yutaka</au><au>Fujii, Tomoyuki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interleukin‐17 is associated with expression of programmed cell death 1 ligand 1 in ovarian carcinoma</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2019-10</date><risdate>2019</risdate><volume>110</volume><issue>10</issue><spage>3068</spage><epage>3078</epage><pages>3068-3078</pages><issn>1347-9032</issn><eissn>1349-7006</eissn><abstract>The programmed cell death 1/programmed cell death 1 ligand 1 pathway was successfully targeted in cancer immunotherapy. Elevated interleukin‐17 (IL‐17), which is known in autoimmune diseases, has recently been recognized in cancer patients. We investigated the role of IL‐17 in the regulation of expression of programmed cell death 1 ligand 1 in ovarian cancer by evaluating changes in the number of IL‐17‐producing cluster of differentiation 4 helper T cells (Th17) and γδT cells (γδT17) in PBMC of 52 gynecological cancer patients (including 30 ovarian cancer patients) and 18 healthy controls. The occupancy ratio of Th17 and γδT17 was higher in ovarian cancer and endometrial cancer patients than in controls, determined by multi‐color flow cytometry (Th17: P < 0.0001 and P = 0.0002, respectively; γδT17: P = 0.0020 and P = 0.0084, respectively). IL‐17 mRNA level was elevated in PBMC of ovarian cancer patients (P = 0.0029), as measured by RT‐PCR. The neutrophil‐to‐lymphocyte ratio, which is a prognostic biomarker of ovarian cancer, correlated with Th17 occupancy ratio in patients (P = 0.0068). We found that programmed cell death 1 ligand 1 expression and its associated factors (IL‐6 and phospho‐signal transducer and activator of transcription 3) were induced by IL‐17 in an ovarian cancer cell line. These results suggest that increased Th17 counts and IL‐17 level, which correlated with high neutrophil‐to‐lymphocyte ratio and programmed cell death 1 ligand 1 expression, are potential biomarkers for poor prognosis in ovarian cancer and likely indications for application of programmed cell death 1 ligand 1 pathway inhibitors.
Although the relationship between IL‐17 and PD‐L1 in ovarian cancer (OC) is not well understood, we found that IL‐17 positively modulates the expression of PD‐L1 and associated factors, IL‐6 and pSTAT3. The number of IL‐17‐producing CD4+ helper T cells (Th17) was positively correlated with the neutrophil‐to‐lymphocyte ratio, which is a prognostic biomarker in OC. Thus, elevated Th17 count and IL‐17 level may predict PD‐L1 overexpression and poor prognosis in OC.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>31432577</pmid><doi>10.1111/cas.14174</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0001-9242-0069</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Wiley-Blackwell Open Access Titles; DOAJ Directory of Open Access Journals; Wiley Online Library Journals Frontfile Complete; PubMed Central |
| subjects | Adult Aged Antigens Apoptosis Autoimmune diseases B7-H1 Antigen - genetics Biomarkers Biotechnology Cancer immunotherapy Case-Control Studies Cell death Cell differentiation Cell Line, Tumor Cervical cancer Chemotherapy Cloning Cytokines Endometrial cancer Endometrial Neoplasms - genetics Endometrial Neoplasms - immunology Endometrium Feedback Female Flow cytometry Gene Expression Regulation, Neoplastic Growth factors Gynecology Helper cells Humans IL‐17 Immunotherapy Infections Interleukin-16 - metabolism Interleukin-17 - genetics Interleukin-17 - metabolism Intraepithelial Lymphocytes - metabolism Ligands Lymphocytes Lymphocytes T Medical prognosis neutrophil‐to‐lymphocyte ratio Original Ovarian cancer Ovarian carcinoma Ovarian Neoplasms - genetics Ovarian Neoplasms - immunology Patients PD-1 protein PD‐L1 Penicillin Peripheral blood mononuclear cells Phosphorylation Plasma Prognosis Signal transduction STAT3 Transcription Factor - metabolism T cell receptors Th17 Th17 Cells - metabolism Transcription Tumor necrosis factor-TNF Tumors Up-Regulation |
| title | Interleukin‐17 is associated with expression of programmed cell death 1 ligand 1 in ovarian carcinoma |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-03T19%3A57%3A09IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Interleukin%E2%80%9017%20is%20associated%20with%20expression%20of%20programmed%20cell%20death%201%20ligand%201%20in%20ovarian%20carcinoma&rft.jtitle=Cancer%20science&rft.au=Aotsuka,%20Aeri&rft.date=2019-10&rft.volume=110&rft.issue=10&rft.spage=3068&rft.epage=3078&rft.pages=3068-3078&rft.issn=1347-9032&rft.eissn=1349-7006&rft_id=info:doi/10.1111/cas.14174&rft_dat=%3Cproquest_pubme%3E2301050001%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2301050001&rft_id=info:pmid/31432577&rfr_iscdi=true |