Inhibition of JNK/STAT3/NF-KB pathway-mediated migration and clonal formation of lung adenocarcinoma A549 cells by daphnetin
Daphnetin, a coumarin derivative isolated from Daphne odorifera, has anti-tumor effects. The MAPK, STAT3, and NF-κB signaling pathways are closely related to the pathogenesis of lung cancer. To investigate the effect of daphnetin on anti-lung adenocarcinoma A549 cells and its mechanism. The anti-tum...
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| Veröffentlicht in: | Cell adhesion & migration 2024-12, Vol.18 (1), p.27-37 |
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| creator | Lv, Zhe Du, Yuna Zhang, Huiqing Fang, Hui Guo, Yujie Zeng, Lifeng Chen, Yiguo Li, Dan Li, Rong |
| description | Daphnetin, a coumarin derivative isolated from Daphne odorifera, has anti-tumor effects. The MAPK, STAT3, and NF-κB signaling pathways are closely related to the pathogenesis of lung cancer. To investigate the effect of daphnetin on anti-lung adenocarcinoma A549 cells and its mechanism. The anti-tumor effects of daphnetin on the proliferation, clone formation, migration, and invasion of A549 lung adenocarcinoma cells were investigated. The results showed that daphnetin inhibited the proliferation, colony formation, migration, and invasion of A549 cells through the MAPK/STAT3/NF-KB pathway, and mainly inhibited the clonal formation and migration of A549 cells through the JNK pathway. These results provide a new research direction and theoretical basis for the use of daphnetin in the inhibition of lung adenocarcinoma. |
| doi_str_mv | 10.1080/19336918.2024.2418049 |
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The MAPK, STAT3, and NF-κB signaling pathways are closely related to the pathogenesis of lung cancer. To investigate the effect of daphnetin on anti-lung adenocarcinoma A549 cells and its mechanism. The anti-tumor effects of daphnetin on the proliferation, clone formation, migration, and invasion of A549 lung adenocarcinoma cells were investigated. The results showed that daphnetin inhibited the proliferation, colony formation, migration, and invasion of A549 cells through the MAPK/STAT3/NF-KB pathway, and mainly inhibited the clonal formation and migration of A549 cells through the JNK pathway. These results provide a new research direction and theoretical basis for the use of daphnetin in the inhibition of lung adenocarcinoma.</description><identifier>ISSN: 1933-6918</identifier><identifier>ISSN: 1933-6926</identifier><identifier>EISSN: 1933-6926</identifier><identifier>DOI: 10.1080/19336918.2024.2418049</identifier><identifier>PMID: 39469948</identifier><language>eng</language><publisher>United States: Taylor & Francis</publisher><subject>A549 Cells ; Adenocarcinoma - drug therapy ; Adenocarcinoma - metabolism ; Adenocarcinoma - pathology ; Adenocarcinoma of Lung - drug therapy ; Adenocarcinoma of Lung - metabolism ; Adenocarcinoma of Lung - pathology ; Cell migration ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; daphnetin ; Humans ; lung adenocarcinoma ; Lung Neoplasms - drug therapy ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; MAP Kinase Signaling System - drug effects ; MAPK ; Neoplasm Invasiveness ; NF-kappa B - metabolism ; Research Paper ; Signal Transduction - drug effects ; STAT3 ; STAT3 Transcription Factor - metabolism ; Umbelliferones - pharmacology</subject><ispartof>Cell adhesion & migration, 2024-12, Vol.18 (1), p.27-37</ispartof><rights>2024 The Author(s). 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Published by Informa UK Limited, trading as Taylor & Francis Group. 2024 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c413t-a33fad31df809956edc6e9bce0fca3a9b97e1940c93a92a9bae2617dd34fe76c3</cites><orcidid>0000-0001-8503-7977</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/PMC11540088/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11540088/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,27502,27924,27925,53791,53793,59143,59144</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39469948$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lv, Zhe</creatorcontrib><creatorcontrib>Du, Yuna</creatorcontrib><creatorcontrib>Zhang, Huiqing</creatorcontrib><creatorcontrib>Fang, Hui</creatorcontrib><creatorcontrib>Guo, Yujie</creatorcontrib><creatorcontrib>Zeng, Lifeng</creatorcontrib><creatorcontrib>Chen, Yiguo</creatorcontrib><creatorcontrib>Li, Dan</creatorcontrib><creatorcontrib>Li, Rong</creatorcontrib><title>Inhibition of JNK/STAT3/NF-KB pathway-mediated migration and clonal formation of lung adenocarcinoma A549 cells by daphnetin</title><title>Cell adhesion & migration</title><addtitle>Cell Adh Migr</addtitle><description>Daphnetin, a coumarin derivative isolated from Daphne odorifera, has anti-tumor effects. The MAPK, STAT3, and NF-κB signaling pathways are closely related to the pathogenesis of lung cancer. To investigate the effect of daphnetin on anti-lung adenocarcinoma A549 cells and its mechanism. The anti-tumor effects of daphnetin on the proliferation, clone formation, migration, and invasion of A549 lung adenocarcinoma cells were investigated. The results showed that daphnetin inhibited the proliferation, colony formation, migration, and invasion of A549 cells through the MAPK/STAT3/NF-KB pathway, and mainly inhibited the clonal formation and migration of A549 cells through the JNK pathway. These results provide a new research direction and theoretical basis for the use of daphnetin in the inhibition of lung adenocarcinoma.</description><subject>A549 Cells</subject><subject>Adenocarcinoma - drug therapy</subject><subject>Adenocarcinoma - metabolism</subject><subject>Adenocarcinoma - pathology</subject><subject>Adenocarcinoma of Lung - drug therapy</subject><subject>Adenocarcinoma of Lung - metabolism</subject><subject>Adenocarcinoma of Lung - pathology</subject><subject>Cell migration</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>daphnetin</subject><subject>Humans</subject><subject>lung adenocarcinoma</subject><subject>Lung Neoplasms - drug therapy</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - pathology</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>MAPK</subject><subject>Neoplasm Invasiveness</subject><subject>NF-kappa B - metabolism</subject><subject>Research Paper</subject><subject>Signal Transduction - drug effects</subject><subject>STAT3</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Umbelliferones - pharmacology</subject><issn>1933-6918</issn><issn>1933-6926</issn><issn>1933-6926</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>0YH</sourceid><sourceid>EIF</sourceid><sourceid>DOA</sourceid><recordid>eNp9kk1vEzEQhlcIREvhJ4B85LKJvf5Y-wShohBalQPhbE1sb-LKawfvhioSP57dfIleONkzfv3MaOYtircETwiWeEoUpUIROalwxSYVIxIz9ay4HPOlUJV4fr4TeVG86roHjLkkQrwsLqhiQikmL4s_87j2S9_7FFFq0Lf72-mPxWxBp_c35e0ntIF-_Qi7snXWQ-8sav0qw14N0SITUoSAmpRbOCHCNq4QWBeTgWx8TC2gGWcKGRdCh5Y7ZGGzjq738XXxooHQuTfH86r4efN5cf21vPv-ZX49uysNI7QvgdIGLCW2kVgpLpw1wqmlcbgxQEEtVe2IYtioIaiGGFwlSG0tZY2rhaFXxfzAtQke9Cb7FvJOJ_B6n0h5pSH33gSnpZSsNrXlygrGDVaE0wpLPkSNY1YNrA8H1ma7HKZiXOwzhCfQpy_Rr_Uq_daEcIaxlAPh_ZGQ06-t63rd-m4cDkSXtp2mpCJckVpWg5QfpCanrsuuOdchWI820Ccb6NEG-miD4d-7f5s8_zrtfRB8PAh83C_vMeVgdQ-7kHKTIRo_9vHfGn8BSovCrg</recordid><startdate>20241231</startdate><enddate>20241231</enddate><creator>Lv, Zhe</creator><creator>Du, Yuna</creator><creator>Zhang, Huiqing</creator><creator>Fang, Hui</creator><creator>Guo, Yujie</creator><creator>Zeng, Lifeng</creator><creator>Chen, Yiguo</creator><creator>Li, Dan</creator><creator>Li, Rong</creator><general>Taylor & Francis</general><general>Taylor & Francis Group</general><scope>0YH</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>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-8503-7977</orcidid></search><sort><creationdate>20241231</creationdate><title>Inhibition of JNK/STAT3/NF-KB pathway-mediated migration and clonal formation of lung adenocarcinoma A549 cells by daphnetin</title><author>Lv, Zhe ; Du, Yuna ; Zhang, Huiqing ; Fang, Hui ; Guo, Yujie ; Zeng, Lifeng ; Chen, Yiguo ; Li, Dan ; Li, Rong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c413t-a33fad31df809956edc6e9bce0fca3a9b97e1940c93a92a9bae2617dd34fe76c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>A549 Cells</topic><topic>Adenocarcinoma - drug therapy</topic><topic>Adenocarcinoma - metabolism</topic><topic>Adenocarcinoma - pathology</topic><topic>Adenocarcinoma of Lung - drug therapy</topic><topic>Adenocarcinoma of Lung - metabolism</topic><topic>Adenocarcinoma of Lung - pathology</topic><topic>Cell migration</topic><topic>Cell Movement - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>daphnetin</topic><topic>Humans</topic><topic>lung adenocarcinoma</topic><topic>Lung Neoplasms - drug therapy</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - pathology</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>MAPK</topic><topic>Neoplasm Invasiveness</topic><topic>NF-kappa B - metabolism</topic><topic>Research Paper</topic><topic>Signal Transduction - drug effects</topic><topic>STAT3</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>Umbelliferones - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lv, Zhe</creatorcontrib><creatorcontrib>Du, Yuna</creatorcontrib><creatorcontrib>Zhang, Huiqing</creatorcontrib><creatorcontrib>Fang, Hui</creatorcontrib><creatorcontrib>Guo, Yujie</creatorcontrib><creatorcontrib>Zeng, Lifeng</creatorcontrib><creatorcontrib>Chen, Yiguo</creatorcontrib><creatorcontrib>Li, Dan</creatorcontrib><creatorcontrib>Li, Rong</creatorcontrib><collection>Access via Taylor & Francis (Open Access Collection)</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cell adhesion & migration</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lv, Zhe</au><au>Du, Yuna</au><au>Zhang, Huiqing</au><au>Fang, Hui</au><au>Guo, Yujie</au><au>Zeng, Lifeng</au><au>Chen, Yiguo</au><au>Li, Dan</au><au>Li, Rong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of JNK/STAT3/NF-KB pathway-mediated migration and clonal formation of lung adenocarcinoma A549 cells by daphnetin</atitle><jtitle>Cell adhesion & migration</jtitle><addtitle>Cell Adh Migr</addtitle><date>2024-12-31</date><risdate>2024</risdate><volume>18</volume><issue>1</issue><spage>27</spage><epage>37</epage><pages>27-37</pages><issn>1933-6918</issn><issn>1933-6926</issn><eissn>1933-6926</eissn><abstract>Daphnetin, a coumarin derivative isolated from Daphne odorifera, has anti-tumor effects. The MAPK, STAT3, and NF-κB signaling pathways are closely related to the pathogenesis of lung cancer. To investigate the effect of daphnetin on anti-lung adenocarcinoma A549 cells and its mechanism. The anti-tumor effects of daphnetin on the proliferation, clone formation, migration, and invasion of A549 lung adenocarcinoma cells were investigated. The results showed that daphnetin inhibited the proliferation, colony formation, migration, and invasion of A549 cells through the MAPK/STAT3/NF-KB pathway, and mainly inhibited the clonal formation and migration of A549 cells through the JNK pathway. These results provide a new research direction and theoretical basis for the use of daphnetin in the inhibition of lung adenocarcinoma.</abstract><cop>United States</cop><pub>Taylor & Francis</pub><pmid>39469948</pmid><doi>10.1080/19336918.2024.2418049</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0001-8503-7977</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | A549 Cells Adenocarcinoma - drug therapy Adenocarcinoma - metabolism Adenocarcinoma - pathology Adenocarcinoma of Lung - drug therapy Adenocarcinoma of Lung - metabolism Adenocarcinoma of Lung - pathology Cell migration Cell Movement - drug effects Cell Proliferation - drug effects daphnetin Humans lung adenocarcinoma Lung Neoplasms - drug therapy Lung Neoplasms - metabolism Lung Neoplasms - pathology MAP Kinase Signaling System - drug effects MAPK Neoplasm Invasiveness NF-kappa B - metabolism Research Paper Signal Transduction - drug effects STAT3 STAT3 Transcription Factor - metabolism Umbelliferones - pharmacology |
| title | Inhibition of JNK/STAT3/NF-KB pathway-mediated migration and clonal formation of lung adenocarcinoma A549 cells by daphnetin |
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