Immunopotentiation effects of apigenin on NK cell proliferation and killing pancreatic cancer cells
Apigenin is a kind of flavonoid with many beneficial biological effects. It not only has direct cytotoxicity to tumor cells, but also can boost the antitumor effect of immune cells by modulating immune system. The purpose of this study was to investigate the proliferation of NK cells treated with ap...
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| Veröffentlicht in: | International journal of immunopathology and pharmacology 2023-01, Vol.37, p.3946320231161174-3946320231161174 |
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| container_title | International journal of immunopathology and pharmacology |
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| creator | Feng, Yong-Bo Chen, Ling Chen, Fu-Xing Yang, Yang Chen, Guo-Hua Zhou, Zhong-Hai Xu, Chun-Fang |
| description | Apigenin is a kind of flavonoid with many beneficial biological effects. It not only has direct cytotoxicity to tumor cells, but also can boost the antitumor effect of immune cells by modulating immune system. The purpose of this study was to investigate the proliferation of NK cells treated with apigenin and its cytotoxicity to pancreatic cancer cells in vitro, and explore its potential molecular mechanism. In this study, the effect of apigenin on NK cell proliferation and killing pancreatic cancer cells were measured by CCK-8 assay. Perforin, granzyme B (Gran B), CD107a, and NKG2D expressions of NK cells induced with apigenin were detected by flow cytometry (FCM). The mRNA expression of Bcl-2, Bax and protein expression of Bcl-2, Bax, p-ERK, and p-JNK in NK cells were evaluated by qRT-PCR and western blotting analysis, respectively. The results showed that appropriate concentration of apigenin could significantly promote the proliferation of NK cells in vitro and enhance the killing activity of NK cells against pancreatic cancer cells. The expressions of surface antigen NKG2D and intracellular antigen perforin and Gran B of NK cells were upregulated after treating with apigenin. Bcl-2 mRNA expression was increased, while Bax mRNA expression was decreased. Similarly, the expression of Bcl-2, p-JNK, and p-ERK protein was upregulated, and the expression of Bax protein was downregulated. The molecular mechanism of the immunopotentiation effects of apigenin may be that it up-regulates Bcl-2 and down-regulates Bax expression at the gene and protein levels to facilitate NK cell proliferation, and up-regulates the expression of perforin, Gran B, and NKG2D through the activation of JNK and ERK pathways to enhance NK cell cytotoxicity. |
| doi_str_mv | 10.1177/03946320231161174 |
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It not only has direct cytotoxicity to tumor cells, but also can boost the antitumor effect of immune cells by modulating immune system. The purpose of this study was to investigate the proliferation of NK cells treated with apigenin and its cytotoxicity to pancreatic cancer cells in vitro, and explore its potential molecular mechanism. In this study, the effect of apigenin on NK cell proliferation and killing pancreatic cancer cells were measured by CCK-8 assay. Perforin, granzyme B (Gran B), CD107a, and NKG2D expressions of NK cells induced with apigenin were detected by flow cytometry (FCM). The mRNA expression of Bcl-2, Bax and protein expression of Bcl-2, Bax, p-ERK, and p-JNK in NK cells were evaluated by qRT-PCR and western blotting analysis, respectively. The results showed that appropriate concentration of apigenin could significantly promote the proliferation of NK cells in vitro and enhance the killing activity of NK cells against pancreatic cancer cells. The expressions of surface antigen NKG2D and intracellular antigen perforin and Gran B of NK cells were upregulated after treating with apigenin. Bcl-2 mRNA expression was increased, while Bax mRNA expression was decreased. Similarly, the expression of Bcl-2, p-JNK, and p-ERK protein was upregulated, and the expression of Bax protein was downregulated. The molecular mechanism of the immunopotentiation effects of apigenin may be that it up-regulates Bcl-2 and down-regulates Bax expression at the gene and protein levels to facilitate NK cell proliferation, and up-regulates the expression of perforin, Gran B, and NKG2D through the activation of JNK and ERK pathways to enhance NK cell cytotoxicity.</description><identifier>ISSN: 0394-6320</identifier><identifier>EISSN: 2058-7384</identifier><identifier>DOI: 10.1177/03946320231161174</identifier><identifier>PMID: 36848930</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Antigens ; Antitumor activity ; Apigenin - pharmacology ; BAX protein ; Bcl-2 protein ; bcl-2-Associated X Protein ; Beta cells ; Cell growth ; Cell Proliferation ; Cholecystokinin ; Cytotoxicity ; Extracellular signal-regulated kinase ; Flavonoids ; Flow cytometry ; Gene expression ; Granzyme B ; Humans ; Immune system ; Molecular modelling ; Natural killer cells ; Natural Killer T-Cells - immunology ; NK Cell Lectin-Like Receptor Subfamily K ; NKG2 antigen ; Original ; Pancreatic cancer ; Pancreatic Neoplasms ; Pancreatic Neoplasms - drug therapy ; Perforin ; Proteins ; Proto-Oncogene Proteins c-bcl-2 ; RNA, Messenger ; Tumor cells ; Western blotting</subject><ispartof>International journal of immunopathology and pharmacology, 2023-01, Vol.37, p.3946320231161174-3946320231161174</ispartof><rights>The Author(s) 2023</rights><rights>The Author(s) 2023. This work is licensed under the Creative Commons Attribution – Non-Commercial License https://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2023 2023 SAGE Publications Ltd unless otherwise noted. Manuscript content on this site is licensed under Creative Commons Licenses</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c466t-2364086d25c1c864a5b030dd7bb8373d42646ef89d06b443f049804e029208963</citedby><cites>FETCH-LOGICAL-c466t-2364086d25c1c864a5b030dd7bb8373d42646ef89d06b443f049804e029208963</cites><orcidid>0000-0003-2460-4696 ; 0000-0001-5618-3940 ; 0000-0003-3683-7200</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/PMC9974612/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9974612/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,21945,27830,27901,27902,44921,45309,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36848930$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Feng, Yong-Bo</creatorcontrib><creatorcontrib>Chen, Ling</creatorcontrib><creatorcontrib>Chen, Fu-Xing</creatorcontrib><creatorcontrib>Yang, Yang</creatorcontrib><creatorcontrib>Chen, Guo-Hua</creatorcontrib><creatorcontrib>Zhou, Zhong-Hai</creatorcontrib><creatorcontrib>Xu, Chun-Fang</creatorcontrib><title>Immunopotentiation effects of apigenin on NK cell proliferation and killing pancreatic cancer cells</title><title>International journal of immunopathology and pharmacology</title><addtitle>Int J Immunopathol Pharmacol</addtitle><description>Apigenin is a kind of flavonoid with many beneficial biological effects. It not only has direct cytotoxicity to tumor cells, but also can boost the antitumor effect of immune cells by modulating immune system. The purpose of this study was to investigate the proliferation of NK cells treated with apigenin and its cytotoxicity to pancreatic cancer cells in vitro, and explore its potential molecular mechanism. In this study, the effect of apigenin on NK cell proliferation and killing pancreatic cancer cells were measured by CCK-8 assay. Perforin, granzyme B (Gran B), CD107a, and NKG2D expressions of NK cells induced with apigenin were detected by flow cytometry (FCM). The mRNA expression of Bcl-2, Bax and protein expression of Bcl-2, Bax, p-ERK, and p-JNK in NK cells were evaluated by qRT-PCR and western blotting analysis, respectively. The results showed that appropriate concentration of apigenin could significantly promote the proliferation of NK cells in vitro and enhance the killing activity of NK cells against pancreatic cancer cells. The expressions of surface antigen NKG2D and intracellular antigen perforin and Gran B of NK cells were upregulated after treating with apigenin. Bcl-2 mRNA expression was increased, while Bax mRNA expression was decreased. Similarly, the expression of Bcl-2, p-JNK, and p-ERK protein was upregulated, and the expression of Bax protein was downregulated. The molecular mechanism of the immunopotentiation effects of apigenin may be that it up-regulates Bcl-2 and down-regulates Bax expression at the gene and protein levels to facilitate NK cell proliferation, and up-regulates the expression of perforin, Gran B, and NKG2D through the activation of JNK and ERK pathways to enhance NK cell cytotoxicity.</description><subject>Antigens</subject><subject>Antitumor activity</subject><subject>Apigenin - pharmacology</subject><subject>BAX protein</subject><subject>Bcl-2 protein</subject><subject>bcl-2-Associated X Protein</subject><subject>Beta cells</subject><subject>Cell growth</subject><subject>Cell Proliferation</subject><subject>Cholecystokinin</subject><subject>Cytotoxicity</subject><subject>Extracellular signal-regulated kinase</subject><subject>Flavonoids</subject><subject>Flow cytometry</subject><subject>Gene expression</subject><subject>Granzyme B</subject><subject>Humans</subject><subject>Immune system</subject><subject>Molecular modelling</subject><subject>Natural killer cells</subject><subject>Natural Killer T-Cells - immunology</subject><subject>NK Cell Lectin-Like Receptor Subfamily K</subject><subject>NKG2 antigen</subject><subject>Original</subject><subject>Pancreatic cancer</subject><subject>Pancreatic Neoplasms</subject><subject>Pancreatic Neoplasms - drug therapy</subject><subject>Perforin</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-bcl-2</subject><subject>RNA, Messenger</subject><subject>Tumor cells</subject><subject>Western blotting</subject><issn>0394-6320</issn><issn>2058-7384</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>AFRWT</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kc1O3TAQha2qVbkCHqCbyhKbbgLjn9jOBqlC0CIQ3bRry3GcW9PETu0EibfH6aW0FHVla-abM3N0EHpH4JgQKU-ANVwwCpQRIkqFv0IbCrWqJFP8Ndqs_WoF9tBhzrcAQIDxWpG3aI8JxVXDYIPs5TguIU5xdmH2ZvYxYNf3zs4Zxx6byW9d8AGX8s0Vtm4Y8JTi4HuXdrAJHf7hh8GHLZ5MsMmVusW2fF36NZAP0JveDNkdPr776NvF-dezz9X1l0-XZx-vK8uFmCvKBAclOlpbYpXgpm6BQdfJtlVMso5TwYXrVdOBaDlnPfBGAXdAGwqqEWwfne50p6UdXWeLo2QGPSU_mnSvo_H6eSf473ob73TTSC4ILQIfHgVS_Lm4POvR59WCCS4uWVOpQAoBUhX06B_0Ni4pFHt6PadmsharINlRNsWck-ufjiGg1xT1ixTLzPu_XTxN_M6sAMc7IJut-7P2_4oP5sykIA</recordid><startdate>20230101</startdate><enddate>20230101</enddate><creator>Feng, Yong-Bo</creator><creator>Chen, Ling</creator><creator>Chen, Fu-Xing</creator><creator>Yang, Yang</creator><creator>Chen, Guo-Hua</creator><creator>Zhou, Zhong-Hai</creator><creator>Xu, Chun-Fang</creator><general>SAGE Publications</general><general>Sage Publications Ltd</general><scope>AFRWT</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>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PKEHL</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-2460-4696</orcidid><orcidid>https://orcid.org/0000-0001-5618-3940</orcidid><orcidid>https://orcid.org/0000-0003-3683-7200</orcidid></search><sort><creationdate>20230101</creationdate><title>Immunopotentiation effects of apigenin on NK cell proliferation and killing pancreatic cancer cells</title><author>Feng, Yong-Bo ; Chen, Ling ; Chen, Fu-Xing ; Yang, Yang ; Chen, Guo-Hua ; Zhou, Zhong-Hai ; Xu, Chun-Fang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c466t-2364086d25c1c864a5b030dd7bb8373d42646ef89d06b443f049804e029208963</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Antigens</topic><topic>Antitumor activity</topic><topic>Apigenin - pharmacology</topic><topic>BAX protein</topic><topic>Bcl-2 protein</topic><topic>bcl-2-Associated X Protein</topic><topic>Beta cells</topic><topic>Cell growth</topic><topic>Cell Proliferation</topic><topic>Cholecystokinin</topic><topic>Cytotoxicity</topic><topic>Extracellular signal-regulated kinase</topic><topic>Flavonoids</topic><topic>Flow cytometry</topic><topic>Gene expression</topic><topic>Granzyme B</topic><topic>Humans</topic><topic>Immune system</topic><topic>Molecular modelling</topic><topic>Natural killer cells</topic><topic>Natural Killer T-Cells - immunology</topic><topic>NK Cell Lectin-Like Receptor Subfamily K</topic><topic>NKG2 antigen</topic><topic>Original</topic><topic>Pancreatic cancer</topic><topic>Pancreatic Neoplasms</topic><topic>Pancreatic Neoplasms - drug therapy</topic><topic>Perforin</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-bcl-2</topic><topic>RNA, Messenger</topic><topic>Tumor cells</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Feng, Yong-Bo</creatorcontrib><creatorcontrib>Chen, Ling</creatorcontrib><creatorcontrib>Chen, Fu-Xing</creatorcontrib><creatorcontrib>Yang, Yang</creatorcontrib><creatorcontrib>Chen, Guo-Hua</creatorcontrib><creatorcontrib>Zhou, Zhong-Hai</creatorcontrib><creatorcontrib>Xu, Chun-Fang</creatorcontrib><collection>Sage Journals GOLD Open Access 2024</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 Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Middle East (New)</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>International journal of immunopathology and pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Feng, Yong-Bo</au><au>Chen, Ling</au><au>Chen, Fu-Xing</au><au>Yang, Yang</au><au>Chen, Guo-Hua</au><au>Zhou, Zhong-Hai</au><au>Xu, Chun-Fang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Immunopotentiation effects of apigenin on NK cell proliferation and killing pancreatic cancer cells</atitle><jtitle>International journal of immunopathology and pharmacology</jtitle><addtitle>Int J Immunopathol Pharmacol</addtitle><date>2023-01-01</date><risdate>2023</risdate><volume>37</volume><spage>3946320231161174</spage><epage>3946320231161174</epage><pages>3946320231161174-3946320231161174</pages><issn>0394-6320</issn><eissn>2058-7384</eissn><abstract>Apigenin is a kind of flavonoid with many beneficial biological effects. It not only has direct cytotoxicity to tumor cells, but also can boost the antitumor effect of immune cells by modulating immune system. The purpose of this study was to investigate the proliferation of NK cells treated with apigenin and its cytotoxicity to pancreatic cancer cells in vitro, and explore its potential molecular mechanism. In this study, the effect of apigenin on NK cell proliferation and killing pancreatic cancer cells were measured by CCK-8 assay. Perforin, granzyme B (Gran B), CD107a, and NKG2D expressions of NK cells induced with apigenin were detected by flow cytometry (FCM). The mRNA expression of Bcl-2, Bax and protein expression of Bcl-2, Bax, p-ERK, and p-JNK in NK cells were evaluated by qRT-PCR and western blotting analysis, respectively. The results showed that appropriate concentration of apigenin could significantly promote the proliferation of NK cells in vitro and enhance the killing activity of NK cells against pancreatic cancer cells. The expressions of surface antigen NKG2D and intracellular antigen perforin and Gran B of NK cells were upregulated after treating with apigenin. Bcl-2 mRNA expression was increased, while Bax mRNA expression was decreased. Similarly, the expression of Bcl-2, p-JNK, and p-ERK protein was upregulated, and the expression of Bax protein was downregulated. The molecular mechanism of the immunopotentiation effects of apigenin may be that it up-regulates Bcl-2 and down-regulates Bax expression at the gene and protein levels to facilitate NK cell proliferation, and up-regulates the expression of perforin, Gran B, and NKG2D through the activation of JNK and ERK pathways to enhance NK cell cytotoxicity.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>36848930</pmid><doi>10.1177/03946320231161174</doi><orcidid>https://orcid.org/0000-0003-2460-4696</orcidid><orcidid>https://orcid.org/0000-0001-5618-3940</orcidid><orcidid>https://orcid.org/0000-0003-3683-7200</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Antigens Antitumor activity Apigenin - pharmacology BAX protein Bcl-2 protein bcl-2-Associated X Protein Beta cells Cell growth Cell Proliferation Cholecystokinin Cytotoxicity Extracellular signal-regulated kinase Flavonoids Flow cytometry Gene expression Granzyme B Humans Immune system Molecular modelling Natural killer cells Natural Killer T-Cells - immunology NK Cell Lectin-Like Receptor Subfamily K NKG2 antigen Original Pancreatic cancer Pancreatic Neoplasms Pancreatic Neoplasms - drug therapy Perforin Proteins Proto-Oncogene Proteins c-bcl-2 RNA, Messenger Tumor cells Western blotting |
| title | Immunopotentiation effects of apigenin on NK cell proliferation and killing pancreatic cancer cells |
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