Honokiol regulates ovarian cancer cell malignant behavior through YAP/TAZ pathway modulation
Background Ovarian cancer (OVCA) stands as one of the most fatal gynecological malignancies. Honokiol (HNK) has been substantiated by numerous studies for its anti‐tumor activity against malignancies including OVCA. Consequently, this work was designed to elucidate the impact of HNK‐mediated modulat...
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| Veröffentlicht in: | The journal of obstetrics and gynaecology research 2024-06, Vol.50 (6), p.1010-1019 |
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| creator | Liu, Fang Zhang, Yufang Xia, Xinyi Han, Jing Cao, Linyan |
| description | Background
Ovarian cancer (OVCA) stands as one of the most fatal gynecological malignancies. Honokiol (HNK) has been substantiated by numerous studies for its anti‐tumor activity against malignancies including OVCA. Consequently, this work was designed to elucidate the impact of HNK‐mediated modulation of the YAP/TAZ pathway on the biological functions of OVCA cells.
Methods
OVCA cells were subjected to treatment with varying concentrations (0, 25, 50, 75, and 100 μM) of HNK, concomitant with the administration of YAP agonist (XMU). Assessment of cellular viability was executed employing the CCK‐8 assay, while quantification of cellular proliferation transpired via colony formation assays. Apoptosis was ascertained using flow cytometry, and expression of apoptosis‐related proteins (caspase‐3, Bcl‐2, Bax), EMT‐related proteins (E‐cadherin, N‐cadherin), migration‐associated proteins (MMP‐2, MMP‐9), and YAP/TAZ pathway‐related proteins was evaluated by western blot. Transwell experiments were conducted to assess cellular migratory and invasive propensities. Xenograft tumor models were built to observe tumor growth (volume and weight), apoptosis was assessed by TUNEL staining, and Ki67 expression was evaluated through IHC.
Results
HNK exerted inhibitory effects on the viability and proliferative capacity of OVCA cells, elicited apoptotic responses, curtailed the migratory and invasive tendencies of cells, and downregulated the YAP/TAZ pathway. Stimulation with YAP agonist (XMU‐MP‐1) partially attenuated the impacts of HNK on OVCA cell biology. Experiments in vivo confirmed that HNK inhibited OVCA tumor growth.
Conclusion
The outcomes of this investigation conclusively established that HNK orchestrated the modulation of the YAP/TAZ pathway, thereby exerting control over the malignant phenotypic manifestations of OVCA cells. The ascertained function of HNK in restraining cellular proliferation and tumor progression provided novel evidence of its anti‐proliferative activity within OVCA cells. |
| doi_str_mv | 10.1111/jog.15940 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_3034245737</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3034245737</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3130-413fab978fb789da8a64ba5ee3eb0b91256a5829de3ce2c56a0c8017fd57d5013</originalsourceid><addsrcrecordid>eNp1kEFLwzAYhoMobk4P_gEJeNFDt6RpmvY4hm6KMA_zoAjla5t2nW0zk3Zj_97MTg-C3yVf4MnDmxehS0qG1M5opfIh5aFHjlCfep5wiOD-sd2ZR52ACL-HzoxZEUJFSINT1GMBFz4ltI_eZ6pWH4UqsZZ5W0IjDVYb0AXUOIE6kRonsixxBWWR11A3OJZL2BRK42apVZsv8ev4ebQYv-E1NMst7HCl0r2oUPU5OsmgNPLicA7Qy_3dYjJznubTh8n4yUkYZcTxKMsgDkWQxSIIUwjA92LgUjIZkzikLveBB26YSpZIN7E3kgT2L1nKRcoJZQN003nXWn220jRRVZh9bKilak3ECPNcjwsmLHr9B12pVtc2naV8RjnzBbfUbUclWhmjZRatdVGB3kWURPvK7as8-q7cslcHYxtXMv0lfzq2wKgDtkUpd_-bosf5tFN-Ab_VipI</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>3063153675</pqid></control><display><type>article</type><title>Honokiol regulates ovarian cancer cell malignant behavior through YAP/TAZ pathway modulation</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><creator>Liu, Fang ; Zhang, Yufang ; Xia, Xinyi ; Han, Jing ; Cao, Linyan</creator><creatorcontrib>Liu, Fang ; Zhang, Yufang ; Xia, Xinyi ; Han, Jing ; Cao, Linyan</creatorcontrib><description>Background
Ovarian cancer (OVCA) stands as one of the most fatal gynecological malignancies. Honokiol (HNK) has been substantiated by numerous studies for its anti‐tumor activity against malignancies including OVCA. Consequently, this work was designed to elucidate the impact of HNK‐mediated modulation of the YAP/TAZ pathway on the biological functions of OVCA cells.
Methods
OVCA cells were subjected to treatment with varying concentrations (0, 25, 50, 75, and 100 μM) of HNK, concomitant with the administration of YAP agonist (XMU). Assessment of cellular viability was executed employing the CCK‐8 assay, while quantification of cellular proliferation transpired via colony formation assays. Apoptosis was ascertained using flow cytometry, and expression of apoptosis‐related proteins (caspase‐3, Bcl‐2, Bax), EMT‐related proteins (E‐cadherin, N‐cadherin), migration‐associated proteins (MMP‐2, MMP‐9), and YAP/TAZ pathway‐related proteins was evaluated by western blot. Transwell experiments were conducted to assess cellular migratory and invasive propensities. Xenograft tumor models were built to observe tumor growth (volume and weight), apoptosis was assessed by TUNEL staining, and Ki67 expression was evaluated through IHC.
Results
HNK exerted inhibitory effects on the viability and proliferative capacity of OVCA cells, elicited apoptotic responses, curtailed the migratory and invasive tendencies of cells, and downregulated the YAP/TAZ pathway. Stimulation with YAP agonist (XMU‐MP‐1) partially attenuated the impacts of HNK on OVCA cell biology. Experiments in vivo confirmed that HNK inhibited OVCA tumor growth.
Conclusion
The outcomes of this investigation conclusively established that HNK orchestrated the modulation of the YAP/TAZ pathway, thereby exerting control over the malignant phenotypic manifestations of OVCA cells. The ascertained function of HNK in restraining cellular proliferation and tumor progression provided novel evidence of its anti‐proliferative activity within OVCA cells.</description><identifier>ISSN: 1341-8076</identifier><identifier>EISSN: 1447-0756</identifier><identifier>DOI: 10.1111/jog.15940</identifier><identifier>PMID: 38576101</identifier><language>eng</language><publisher>Kyoto, Japan: John Wiley & Sons Australia, Ltd</publisher><subject>Adaptor Proteins, Signal Transducing - metabolism ; Agonists ; Allyl Compounds ; Animals ; Antineoplastic Agents, Phytogenic - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Biphenyl Compounds - pharmacology ; Caspase ; Cell Line, Tumor ; Cell Movement - drug effects ; Cell proliferation ; Cell Proliferation - drug effects ; Cell viability ; Cholecystokinin ; Female ; Flow cytometry ; honokiol ; Humans ; inhibit ; Invasiveness ; Lignans - pharmacology ; Malignancy ; malignant behavior ; Mice ; Mice, Nude ; Ovarian cancer ; Ovarian Neoplasms - drug therapy ; Ovarian Neoplasms - metabolism ; Ovarian Neoplasms - pathology ; Phenols ; Proteins ; Signal Transduction - drug effects ; Transcription Factors - metabolism ; Transcriptional Coactivator with PDZ-Binding Motif Proteins ; Tumors ; Xenograft Model Antitumor Assays ; YAP-Signaling Proteins ; YAP/TAZ ; Yes-associated protein</subject><ispartof>The journal of obstetrics and gynaecology research, 2024-06, Vol.50 (6), p.1010-1019</ispartof><rights>2024 Japan Society of Obstetrics and Gynecology.</rights><rights>2024 Japan Society of Obstetrics and Gynecology</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c3130-413fab978fb789da8a64ba5ee3eb0b91256a5829de3ce2c56a0c8017fd57d5013</cites><orcidid>0009-0004-5222-0221</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fjog.15940$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fjog.15940$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27926,27927,45576,45577</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38576101$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Fang</creatorcontrib><creatorcontrib>Zhang, Yufang</creatorcontrib><creatorcontrib>Xia, Xinyi</creatorcontrib><creatorcontrib>Han, Jing</creatorcontrib><creatorcontrib>Cao, Linyan</creatorcontrib><title>Honokiol regulates ovarian cancer cell malignant behavior through YAP/TAZ pathway modulation</title><title>The journal of obstetrics and gynaecology research</title><addtitle>J Obstet Gynaecol Res</addtitle><description>Background
Ovarian cancer (OVCA) stands as one of the most fatal gynecological malignancies. Honokiol (HNK) has been substantiated by numerous studies for its anti‐tumor activity against malignancies including OVCA. Consequently, this work was designed to elucidate the impact of HNK‐mediated modulation of the YAP/TAZ pathway on the biological functions of OVCA cells.
Methods
OVCA cells were subjected to treatment with varying concentrations (0, 25, 50, 75, and 100 μM) of HNK, concomitant with the administration of YAP agonist (XMU). Assessment of cellular viability was executed employing the CCK‐8 assay, while quantification of cellular proliferation transpired via colony formation assays. Apoptosis was ascertained using flow cytometry, and expression of apoptosis‐related proteins (caspase‐3, Bcl‐2, Bax), EMT‐related proteins (E‐cadherin, N‐cadherin), migration‐associated proteins (MMP‐2, MMP‐9), and YAP/TAZ pathway‐related proteins was evaluated by western blot. Transwell experiments were conducted to assess cellular migratory and invasive propensities. Xenograft tumor models were built to observe tumor growth (volume and weight), apoptosis was assessed by TUNEL staining, and Ki67 expression was evaluated through IHC.
Results
HNK exerted inhibitory effects on the viability and proliferative capacity of OVCA cells, elicited apoptotic responses, curtailed the migratory and invasive tendencies of cells, and downregulated the YAP/TAZ pathway. Stimulation with YAP agonist (XMU‐MP‐1) partially attenuated the impacts of HNK on OVCA cell biology. Experiments in vivo confirmed that HNK inhibited OVCA tumor growth.
Conclusion
The outcomes of this investigation conclusively established that HNK orchestrated the modulation of the YAP/TAZ pathway, thereby exerting control over the malignant phenotypic manifestations of OVCA cells. The ascertained function of HNK in restraining cellular proliferation and tumor progression provided novel evidence of its anti‐proliferative activity within OVCA cells.</description><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Agonists</subject><subject>Allyl Compounds</subject><subject>Animals</subject><subject>Antineoplastic Agents, Phytogenic - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Biphenyl Compounds - pharmacology</subject><subject>Caspase</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell viability</subject><subject>Cholecystokinin</subject><subject>Female</subject><subject>Flow cytometry</subject><subject>honokiol</subject><subject>Humans</subject><subject>inhibit</subject><subject>Invasiveness</subject><subject>Lignans - pharmacology</subject><subject>Malignancy</subject><subject>malignant behavior</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Ovarian cancer</subject><subject>Ovarian Neoplasms - drug therapy</subject><subject>Ovarian Neoplasms - metabolism</subject><subject>Ovarian Neoplasms - pathology</subject><subject>Phenols</subject><subject>Proteins</subject><subject>Signal Transduction - drug effects</subject><subject>Transcription Factors - metabolism</subject><subject>Transcriptional Coactivator with PDZ-Binding Motif Proteins</subject><subject>Tumors</subject><subject>Xenograft Model Antitumor Assays</subject><subject>YAP-Signaling Proteins</subject><subject>YAP/TAZ</subject><subject>Yes-associated protein</subject><issn>1341-8076</issn><issn>1447-0756</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kEFLwzAYhoMobk4P_gEJeNFDt6RpmvY4hm6KMA_zoAjla5t2nW0zk3Zj_97MTg-C3yVf4MnDmxehS0qG1M5opfIh5aFHjlCfep5wiOD-sd2ZR52ACL-HzoxZEUJFSINT1GMBFz4ltI_eZ6pWH4UqsZZ5W0IjDVYb0AXUOIE6kRonsixxBWWR11A3OJZL2BRK42apVZsv8ev4ebQYv-E1NMst7HCl0r2oUPU5OsmgNPLicA7Qy_3dYjJznubTh8n4yUkYZcTxKMsgDkWQxSIIUwjA92LgUjIZkzikLveBB26YSpZIN7E3kgT2L1nKRcoJZQN003nXWn220jRRVZh9bKilak3ECPNcjwsmLHr9B12pVtc2naV8RjnzBbfUbUclWhmjZRatdVGB3kWURPvK7as8-q7cslcHYxtXMv0lfzq2wKgDtkUpd_-bosf5tFN-Ab_VipI</recordid><startdate>202406</startdate><enddate>202406</enddate><creator>Liu, Fang</creator><creator>Zhang, Yufang</creator><creator>Xia, Xinyi</creator><creator>Han, Jing</creator><creator>Cao, Linyan</creator><general>John Wiley & Sons Australia, Ltd</general><general>Wiley Subscription Services, Inc</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>7T5</scope><scope>7TO</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0009-0004-5222-0221</orcidid></search><sort><creationdate>202406</creationdate><title>Honokiol regulates ovarian cancer cell malignant behavior through YAP/TAZ pathway modulation</title><author>Liu, Fang ; Zhang, Yufang ; Xia, Xinyi ; Han, Jing ; Cao, Linyan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3130-413fab978fb789da8a64ba5ee3eb0b91256a5829de3ce2c56a0c8017fd57d5013</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Adaptor Proteins, Signal Transducing - metabolism</topic><topic>Agonists</topic><topic>Allyl Compounds</topic><topic>Animals</topic><topic>Antineoplastic Agents, Phytogenic - pharmacology</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Biphenyl Compounds - pharmacology</topic><topic>Caspase</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - drug effects</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell viability</topic><topic>Cholecystokinin</topic><topic>Female</topic><topic>Flow cytometry</topic><topic>honokiol</topic><topic>Humans</topic><topic>inhibit</topic><topic>Invasiveness</topic><topic>Lignans - pharmacology</topic><topic>Malignancy</topic><topic>malignant behavior</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Ovarian cancer</topic><topic>Ovarian Neoplasms - drug therapy</topic><topic>Ovarian Neoplasms - metabolism</topic><topic>Ovarian Neoplasms - pathology</topic><topic>Phenols</topic><topic>Proteins</topic><topic>Signal Transduction - drug effects</topic><topic>Transcription Factors - metabolism</topic><topic>Transcriptional Coactivator with PDZ-Binding Motif Proteins</topic><topic>Tumors</topic><topic>Xenograft Model Antitumor Assays</topic><topic>YAP-Signaling Proteins</topic><topic>YAP/TAZ</topic><topic>Yes-associated protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Fang</creatorcontrib><creatorcontrib>Zhang, Yufang</creatorcontrib><creatorcontrib>Xia, Xinyi</creatorcontrib><creatorcontrib>Han, Jing</creatorcontrib><creatorcontrib>Cao, Linyan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>The journal of obstetrics and gynaecology research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Fang</au><au>Zhang, Yufang</au><au>Xia, Xinyi</au><au>Han, Jing</au><au>Cao, Linyan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Honokiol regulates ovarian cancer cell malignant behavior through YAP/TAZ pathway modulation</atitle><jtitle>The journal of obstetrics and gynaecology research</jtitle><addtitle>J Obstet Gynaecol Res</addtitle><date>2024-06</date><risdate>2024</risdate><volume>50</volume><issue>6</issue><spage>1010</spage><epage>1019</epage><pages>1010-1019</pages><issn>1341-8076</issn><eissn>1447-0756</eissn><abstract>Background
Ovarian cancer (OVCA) stands as one of the most fatal gynecological malignancies. Honokiol (HNK) has been substantiated by numerous studies for its anti‐tumor activity against malignancies including OVCA. Consequently, this work was designed to elucidate the impact of HNK‐mediated modulation of the YAP/TAZ pathway on the biological functions of OVCA cells.
Methods
OVCA cells were subjected to treatment with varying concentrations (0, 25, 50, 75, and 100 μM) of HNK, concomitant with the administration of YAP agonist (XMU). Assessment of cellular viability was executed employing the CCK‐8 assay, while quantification of cellular proliferation transpired via colony formation assays. Apoptosis was ascertained using flow cytometry, and expression of apoptosis‐related proteins (caspase‐3, Bcl‐2, Bax), EMT‐related proteins (E‐cadherin, N‐cadherin), migration‐associated proteins (MMP‐2, MMP‐9), and YAP/TAZ pathway‐related proteins was evaluated by western blot. Transwell experiments were conducted to assess cellular migratory and invasive propensities. Xenograft tumor models were built to observe tumor growth (volume and weight), apoptosis was assessed by TUNEL staining, and Ki67 expression was evaluated through IHC.
Results
HNK exerted inhibitory effects on the viability and proliferative capacity of OVCA cells, elicited apoptotic responses, curtailed the migratory and invasive tendencies of cells, and downregulated the YAP/TAZ pathway. Stimulation with YAP agonist (XMU‐MP‐1) partially attenuated the impacts of HNK on OVCA cell biology. Experiments in vivo confirmed that HNK inhibited OVCA tumor growth.
Conclusion
The outcomes of this investigation conclusively established that HNK orchestrated the modulation of the YAP/TAZ pathway, thereby exerting control over the malignant phenotypic manifestations of OVCA cells. The ascertained function of HNK in restraining cellular proliferation and tumor progression provided novel evidence of its anti‐proliferative activity within OVCA cells.</abstract><cop>Kyoto, Japan</cop><pub>John Wiley & Sons Australia, Ltd</pub><pmid>38576101</pmid><doi>10.1111/jog.15940</doi><tpages>10</tpages><orcidid>https://orcid.org/0009-0004-5222-0221</orcidid></addata></record> |
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| subjects | Adaptor Proteins, Signal Transducing - metabolism Agonists Allyl Compounds Animals Antineoplastic Agents, Phytogenic - pharmacology Apoptosis Apoptosis - drug effects Biphenyl Compounds - pharmacology Caspase Cell Line, Tumor Cell Movement - drug effects Cell proliferation Cell Proliferation - drug effects Cell viability Cholecystokinin Female Flow cytometry honokiol Humans inhibit Invasiveness Lignans - pharmacology Malignancy malignant behavior Mice Mice, Nude Ovarian cancer Ovarian Neoplasms - drug therapy Ovarian Neoplasms - metabolism Ovarian Neoplasms - pathology Phenols Proteins Signal Transduction - drug effects Transcription Factors - metabolism Transcriptional Coactivator with PDZ-Binding Motif Proteins Tumors Xenograft Model Antitumor Assays YAP-Signaling Proteins YAP/TAZ Yes-associated protein |
| title | Honokiol regulates ovarian cancer cell malignant behavior through YAP/TAZ pathway modulation |
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