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Genipin promotes the apoptosis and autophagy of neuroblastoma cells by suppressing the PI3K/AKT/mTOR pathway
This study investigated the underlying function and mechanism of genipin in neuroblastoma (NB). Using flow cytometry analysis and cytotoxicity tests, in vitro studies were conducted to assess the effects of genipin on the SK-N-SH cell line. The mechanism of action of genipin was explored through imm...
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| Published in: | Scientific reports 2024-08, Vol.14 (1), p.20231-20, Article 20231 |
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| creator | Liu, Xinying Zhou, Can Cheng, Boli Xiong, Yan Zhou, Qin Wan, Enyu He, Yun |
| description | This study investigated the underlying function and mechanism of genipin in neuroblastoma (NB). Using flow cytometry analysis and cytotoxicity tests, in vitro studies were conducted to assess the effects of genipin on the SK-N-SH cell line. The mechanism of action of genipin was explored through immunofluorescence staining, Western blotting, and caspase-3 activity assays. In addition, we also created a xenograft tumour model to investigate the effects of genipin in vivo. This research confirmed that genipin suppressed cell viability, induced apoptosis, and promoted autophagy, processes that are likely linked to the inhibition of the PI3K/AKT/mTOR signalling pathway. Autophagy inhibition increases the sensitivity of SK-N-SH cells to genipin. Furthermore, combination treatment with a PI3K inhibitor enhanced the therapeutic efficacy of genipin. These results highlight the potential of genipin as a candidate drug for the treatment of NB. |
| doi_str_mv | 10.1038/s41598-024-71123-w |
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Using flow cytometry analysis and cytotoxicity tests, in vitro studies were conducted to assess the effects of genipin on the SK-N-SH cell line. The mechanism of action of genipin was explored through immunofluorescence staining, Western blotting, and caspase-3 activity assays. In addition, we also created a xenograft tumour model to investigate the effects of genipin in vivo. This research confirmed that genipin suppressed cell viability, induced apoptosis, and promoted autophagy, processes that are likely linked to the inhibition of the PI3K/AKT/mTOR signalling pathway. Autophagy inhibition increases the sensitivity of SK-N-SH cells to genipin. Furthermore, combination treatment with a PI3K inhibitor enhanced the therapeutic efficacy of genipin. These results highlight the potential of genipin as a candidate drug for the treatment of NB.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-024-71123-w</identifier><identifier>PMID: 39215133</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>1-Phosphatidylinositol 3-kinase ; 631/67 ; 631/67/1059 ; 631/67/1059/153 ; 631/67/2332 ; AKT protein ; Animals ; Apoptosis ; Apoptosis - drug effects ; Autophagy ; Autophagy - drug effects ; Cancer therapies ; Caspase-3 ; Cell Line, Tumor ; Cell Survival - drug effects ; Cell viability ; Cytotoxicity ; Drug resistance ; Flow cytometry ; Genipin ; Humanities and Social Sciences ; Humans ; Immunofluorescence ; Iridoids - pharmacology ; Kinases ; Medical prognosis ; Medical schools ; Metabolism ; Mice ; multidisciplinary ; Natural products ; Neuroblastoma ; Neuroblastoma - drug therapy ; Neuroblastoma - metabolism ; Neuroblastoma - pathology ; Neuroblasts ; Pediatrics ; Phosphatidylinositol 3-Kinases - metabolism ; Proteins ; Proto-Oncogene Proteins c-akt - metabolism ; Radiation ; Science ; Science (multidisciplinary) ; Signal transduction ; Signal Transduction - drug effects ; TOR protein ; TOR Serine-Threonine Kinases - metabolism ; Tumors ; Western blotting ; Xenograft Model Antitumor Assays</subject><ispartof>Scientific reports, 2024-08, Vol.14 (1), p.20231-20, Article 20231</ispartof><rights>The Author(s) 2024</rights><rights>2024. The Author(s).</rights><rights>The Author(s) 2024. 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><cites>FETCH-LOGICAL-c366t-4084ee4ba5a7531a802d7e148d41fb6408ce2e116f9b5bb8a1a8005f463af5b83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/3098953514/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/3098953514?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,25753,27924,27925,37012,37013,44590,74998</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39215133$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Xinying</creatorcontrib><creatorcontrib>Zhou, Can</creatorcontrib><creatorcontrib>Cheng, Boli</creatorcontrib><creatorcontrib>Xiong, Yan</creatorcontrib><creatorcontrib>Zhou, Qin</creatorcontrib><creatorcontrib>Wan, Enyu</creatorcontrib><creatorcontrib>He, Yun</creatorcontrib><title>Genipin promotes the apoptosis and autophagy of neuroblastoma cells by suppressing the PI3K/AKT/mTOR pathway</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>This study investigated the underlying function and mechanism of genipin in neuroblastoma (NB). Using flow cytometry analysis and cytotoxicity tests, in vitro studies were conducted to assess the effects of genipin on the SK-N-SH cell line. The mechanism of action of genipin was explored through immunofluorescence staining, Western blotting, and caspase-3 activity assays. In addition, we also created a xenograft tumour model to investigate the effects of genipin in vivo. This research confirmed that genipin suppressed cell viability, induced apoptosis, and promoted autophagy, processes that are likely linked to the inhibition of the PI3K/AKT/mTOR signalling pathway. Autophagy inhibition increases the sensitivity of SK-N-SH cells to genipin. Furthermore, combination treatment with a PI3K inhibitor enhanced the therapeutic efficacy of genipin. These results highlight the potential of genipin as a candidate drug for the treatment of NB.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>631/67</subject><subject>631/67/1059</subject><subject>631/67/1059/153</subject><subject>631/67/2332</subject><subject>AKT protein</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Autophagy</subject><subject>Autophagy - drug effects</subject><subject>Cancer therapies</subject><subject>Caspase-3</subject><subject>Cell Line, Tumor</subject><subject>Cell Survival - drug effects</subject><subject>Cell viability</subject><subject>Cytotoxicity</subject><subject>Drug resistance</subject><subject>Flow cytometry</subject><subject>Genipin</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Immunofluorescence</subject><subject>Iridoids - pharmacology</subject><subject>Kinases</subject><subject>Medical prognosis</subject><subject>Medical schools</subject><subject>Metabolism</subject><subject>Mice</subject><subject>multidisciplinary</subject><subject>Natural products</subject><subject>Neuroblastoma</subject><subject>Neuroblastoma - drug therapy</subject><subject>Neuroblastoma - metabolism</subject><subject>Neuroblastoma - pathology</subject><subject>Neuroblasts</subject><subject>Pediatrics</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Radiation</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>TOR protein</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><subject>Tumors</subject><subject>Western blotting</subject><subject>Xenograft Model Antitumor Assays</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNp9kc1u1DAURiMEolXpC7BAltiwCePfxF5WFS2jVipCw9q6SW5mMkriYDsazdvjmZSCWOCNLd_jY19_Wfae0c-MCr0Kkimjc8plXjLGRX54lV1yKlXOBeev_1pfZNch7GkaihvJzNvsQhjOFBPiMuvvceymbiSTd4OLGEjcIYHJTdGFLhAYGwJzdNMOtkfiWjLi7F3VQ4huAFJj3wdSHUmYp8ljCN24PRu-rcXD6uZhsxo2T9_JBHF3gOO77E0LfcDr5_kq-3H3ZXP7NX98ul_f3jzmtSiKmEuqJaKsQEGpBANNeVMik7qRrK2KVK6RI2NFaypVVRpOCFWtLAS0qtLiKlsv3sbB3k6-G8AfrYPOnjec31rwsat7tKi5QV5gwxsqyxaMEU3LSoOGFgUomlyfFlf6oJ8zhmiHLpzahhHdHKygxmhaKKMS-vEfdO9mP6ZOT5ROhGIyUXyhau9C8Ni-PJBRe4rWLtHaFK09R2sP6dCHZ_VcDdi8HPkdZALEAoRUGrfo_9z9H-0vvHOuVA</recordid><startdate>20240830</startdate><enddate>20240830</enddate><creator>Liu, Xinying</creator><creator>Zhou, Can</creator><creator>Cheng, Boli</creator><creator>Xiong, Yan</creator><creator>Zhou, Qin</creator><creator>Wan, Enyu</creator><creator>He, Yun</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><general>Nature Portfolio</general><scope>C6C</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>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>DOA</scope></search><sort><creationdate>20240830</creationdate><title>Genipin promotes the apoptosis and autophagy of neuroblastoma cells by suppressing the PI3K/AKT/mTOR pathway</title><author>Liu, Xinying ; Zhou, Can ; Cheng, Boli ; Xiong, Yan ; Zhou, Qin ; Wan, Enyu ; He, Yun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c366t-4084ee4ba5a7531a802d7e148d41fb6408ce2e116f9b5bb8a1a8005f463af5b83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>631/67</topic><topic>631/67/1059</topic><topic>631/67/1059/153</topic><topic>631/67/2332</topic><topic>AKT protein</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Autophagy</topic><topic>Autophagy - drug effects</topic><topic>Cancer therapies</topic><topic>Caspase-3</topic><topic>Cell Line, Tumor</topic><topic>Cell Survival - drug effects</topic><topic>Cell viability</topic><topic>Cytotoxicity</topic><topic>Drug resistance</topic><topic>Flow cytometry</topic><topic>Genipin</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Immunofluorescence</topic><topic>Iridoids - pharmacology</topic><topic>Kinases</topic><topic>Medical prognosis</topic><topic>Medical schools</topic><topic>Metabolism</topic><topic>Mice</topic><topic>multidisciplinary</topic><topic>Natural products</topic><topic>Neuroblastoma</topic><topic>Neuroblastoma - drug therapy</topic><topic>Neuroblastoma - metabolism</topic><topic>Neuroblastoma - pathology</topic><topic>Neuroblasts</topic><topic>Pediatrics</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Radiation</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>TOR protein</topic><topic>TOR Serine-Threonine Kinases - metabolism</topic><topic>Tumors</topic><topic>Western blotting</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Xinying</creatorcontrib><creatorcontrib>Zhou, Can</creatorcontrib><creatorcontrib>Cheng, Boli</creatorcontrib><creatorcontrib>Xiong, Yan</creatorcontrib><creatorcontrib>Zhou, Qin</creatorcontrib><creatorcontrib>Wan, Enyu</creatorcontrib><creatorcontrib>He, Yun</creatorcontrib><collection>Springer Nature OA Free Journals</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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 One Sustainability</collection><collection>ProQuest Central</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</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Science Database</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Xinying</au><au>Zhou, Can</au><au>Cheng, Boli</au><au>Xiong, Yan</au><au>Zhou, Qin</au><au>Wan, Enyu</au><au>He, Yun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genipin promotes the apoptosis and autophagy of neuroblastoma cells by suppressing the PI3K/AKT/mTOR pathway</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2024-08-30</date><risdate>2024</risdate><volume>14</volume><issue>1</issue><spage>20231</spage><epage>20</epage><pages>20231-20</pages><artnum>20231</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>This study investigated the underlying function and mechanism of genipin in neuroblastoma (NB). Using flow cytometry analysis and cytotoxicity tests, in vitro studies were conducted to assess the effects of genipin on the SK-N-SH cell line. The mechanism of action of genipin was explored through immunofluorescence staining, Western blotting, and caspase-3 activity assays. In addition, we also created a xenograft tumour model to investigate the effects of genipin in vivo. This research confirmed that genipin suppressed cell viability, induced apoptosis, and promoted autophagy, processes that are likely linked to the inhibition of the PI3K/AKT/mTOR signalling pathway. Autophagy inhibition increases the sensitivity of SK-N-SH cells to genipin. Furthermore, combination treatment with a PI3K inhibitor enhanced the therapeutic efficacy of genipin. These results highlight the potential of genipin as a candidate drug for the treatment of NB.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>39215133</pmid><doi>10.1038/s41598-024-71123-w</doi><tpages>20</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase 631/67 631/67/1059 631/67/1059/153 631/67/2332 AKT protein Animals Apoptosis Apoptosis - drug effects Autophagy Autophagy - drug effects Cancer therapies Caspase-3 Cell Line, Tumor Cell Survival - drug effects Cell viability Cytotoxicity Drug resistance Flow cytometry Genipin Humanities and Social Sciences Humans Immunofluorescence Iridoids - pharmacology Kinases Medical prognosis Medical schools Metabolism Mice multidisciplinary Natural products Neuroblastoma Neuroblastoma - drug therapy Neuroblastoma - metabolism Neuroblastoma - pathology Neuroblasts Pediatrics Phosphatidylinositol 3-Kinases - metabolism Proteins Proto-Oncogene Proteins c-akt - metabolism Radiation Science Science (multidisciplinary) Signal transduction Signal Transduction - drug effects TOR protein TOR Serine-Threonine Kinases - metabolism Tumors Western blotting Xenograft Model Antitumor Assays |
| title | Genipin promotes the apoptosis and autophagy of neuroblastoma cells by suppressing the PI3K/AKT/mTOR pathway |
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