Autophagy mediates cytotoxicity of human colorectal cancer cells treated with garcinielliptone FC
The tautomeric pair of garcinielliptone FC (GFC) is a novel tautomeric pair of polyprenyl benzophenonoid isolated from the pericarps of Garcinia subelliptica Merr. (G. subelliptica, Clusiaceae), a tree with abundant sources of polyphenols. Our previous report demonstrated that GFC induced apoptosis...
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| Veröffentlicht in: | Journal of cellular physiology 2018-01, Vol.233 (1), p.497-505 |
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| creator | Won, Shen‐Jeu Yen, Cheng‐Hsin Lin, Ting‐Yu Jiang‐Shieh, Ya‐Fen Lin, Chun‐Nan Chen, Jyun‐Ti Su, Chun‐Li |
| description | The tautomeric pair of garcinielliptone FC (GFC) is a novel tautomeric pair of polyprenyl benzophenonoid isolated from the pericarps of Garcinia subelliptica Merr. (G. subelliptica, Clusiaceae), a tree with abundant sources of polyphenols. Our previous report demonstrated that GFC induced apoptosis on various types of human cancer cell lines including chemoresistant human colorectal cancer HT‐29 cells. In the present study, we observed that many autophagy‐related genes in GFC‐treated HT‐29 cells were up‐ and down‐regulated using a cDNA microarray containing oncogenes and kinase genes. GFC‐induced autophagy of HT‐29 cells was confirmed by observing the formation of acidic vesicular organelles, LC3 puncta, and double‐membrane autophagic vesicles using flow cytometry, confocal microscopy, and transmission electron microscopy, respectively. Inhibition of AKT/mTOR/P70S6K signaling as well as formation of Atg5‐Atg12 and PI3K/Beclin‐1 complexes were observed using Western blot. Administration of autophagy inhibitor (3‐methyladenine and shRNA Atg5) and apoptosis inhibitor Z‐VAD showed that the GFC‐induced autophagy was cytotoxic form and GFC‐induced apoptosis enhanced GFC‐induced autophagy. Our data suggest the involvement of autophagy and apoptosis in GFC‐induced anticancer mechanisms of human colorectal cancer.
The tautomeric pair of garcinielliptone FC (GFC) is a novel tautomeric pair of polyprenyl benzophenonoid isolated from the pericarps of Garcinia subelliptica Merr. (G. subelliptica, Clusiaceae), a tree with abundant sources of polyphenols. GFC‐induced autophagy was cytotoxic form and GFC‐induced apoptosis enhanced GFC‐induced autophagy. |
| doi_str_mv | 10.1002/jcp.25910 |
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The tautomeric pair of garcinielliptone FC (GFC) is a novel tautomeric pair of polyprenyl benzophenonoid isolated from the pericarps of Garcinia subelliptica Merr. (G. subelliptica, Clusiaceae), a tree with abundant sources of polyphenols. GFC‐induced autophagy was cytotoxic form and GFC‐induced apoptosis enhanced GFC‐induced autophagy.</description><identifier>ISSN: 0021-9541</identifier><identifier>EISSN: 1097-4652</identifier><identifier>DOI: 10.1002/jcp.25910</identifier><identifier>PMID: 28294332</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Antineoplastic Agents, Phytogenic - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Autophagy ; Autophagy - drug effects ; Autophagy-Related Protein 12 - genetics ; Autophagy-Related Protein 12 - metabolism ; Autophagy-Related Protein 5 - genetics ; Autophagy-Related Protein 5 - metabolism ; Beclin-1 - genetics ; Beclin-1 - metabolism ; Cancer ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - drug therapy ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - metabolism ; Colorectal Neoplasms - ultrastructure ; Confocal microscopy ; Cytometry ; Cytotoxicity ; DNA microarrays ; Dose-Response Relationship, Drug ; Electron microscopy ; Flow cytometry ; garcinielliptone FC ; Gene Expression Regulation, Neoplastic ; Genes ; HT29 Cells ; human colorectal cancer ; Humans ; Inhibitors ; Membrane vesicles ; Organelles ; Phagocytosis ; Phosphatidylinositol 3-Kinase - metabolism ; Polyphenols ; Proto-Oncogene Proteins c-akt - metabolism ; Ribosomal Protein S6 Kinases, 70-kDa - metabolism ; RNA Interference ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Signal Transduction - drug effects ; Time Factors ; TOR protein ; TOR Serine-Threonine Kinases - metabolism ; Toxicity ; Transfection ; Transmission electron microscopy ; Triterpenes - pharmacology ; Tumor cell lines</subject><ispartof>Journal of cellular physiology, 2018-01, Vol.233 (1), p.497-505</ispartof><rights>2017 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3530-b45654b39d189166ecac23e66ef2ab6cf6837b1ae1f743ecd14e137c8b6d57b03</citedby><cites>FETCH-LOGICAL-c3530-b45654b39d189166ecac23e66ef2ab6cf6837b1ae1f743ecd14e137c8b6d57b03</cites><orcidid>0000-0001-7617-2077</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcp.25910$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcp.25910$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28294332$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Won, Shen‐Jeu</creatorcontrib><creatorcontrib>Yen, Cheng‐Hsin</creatorcontrib><creatorcontrib>Lin, Ting‐Yu</creatorcontrib><creatorcontrib>Jiang‐Shieh, Ya‐Fen</creatorcontrib><creatorcontrib>Lin, Chun‐Nan</creatorcontrib><creatorcontrib>Chen, Jyun‐Ti</creatorcontrib><creatorcontrib>Su, Chun‐Li</creatorcontrib><title>Autophagy mediates cytotoxicity of human colorectal cancer cells treated with garcinielliptone FC</title><title>Journal of cellular physiology</title><addtitle>J Cell Physiol</addtitle><description>The tautomeric pair of garcinielliptone FC (GFC) is a novel tautomeric pair of polyprenyl benzophenonoid isolated from the pericarps of Garcinia subelliptica Merr. (G. subelliptica, Clusiaceae), a tree with abundant sources of polyphenols. Our previous report demonstrated that GFC induced apoptosis on various types of human cancer cell lines including chemoresistant human colorectal cancer HT‐29 cells. In the present study, we observed that many autophagy‐related genes in GFC‐treated HT‐29 cells were up‐ and down‐regulated using a cDNA microarray containing oncogenes and kinase genes. GFC‐induced autophagy of HT‐29 cells was confirmed by observing the formation of acidic vesicular organelles, LC3 puncta, and double‐membrane autophagic vesicles using flow cytometry, confocal microscopy, and transmission electron microscopy, respectively. Inhibition of AKT/mTOR/P70S6K signaling as well as formation of Atg5‐Atg12 and PI3K/Beclin‐1 complexes were observed using Western blot. Administration of autophagy inhibitor (3‐methyladenine and shRNA Atg5) and apoptosis inhibitor Z‐VAD showed that the GFC‐induced autophagy was cytotoxic form and GFC‐induced apoptosis enhanced GFC‐induced autophagy. Our data suggest the involvement of autophagy and apoptosis in GFC‐induced anticancer mechanisms of human colorectal cancer.
The tautomeric pair of garcinielliptone FC (GFC) is a novel tautomeric pair of polyprenyl benzophenonoid isolated from the pericarps of Garcinia subelliptica Merr. (G. subelliptica, Clusiaceae), a tree with abundant sources of polyphenols. GFC‐induced autophagy was cytotoxic form and GFC‐induced apoptosis enhanced GFC‐induced autophagy.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Antineoplastic Agents, Phytogenic - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Autophagy</subject><subject>Autophagy - drug effects</subject><subject>Autophagy-Related Protein 12 - genetics</subject><subject>Autophagy-Related Protein 12 - metabolism</subject><subject>Autophagy-Related Protein 5 - genetics</subject><subject>Autophagy-Related Protein 5 - metabolism</subject><subject>Beclin-1 - genetics</subject><subject>Beclin-1 - metabolism</subject><subject>Cancer</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - drug therapy</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - metabolism</subject><subject>Colorectal Neoplasms - ultrastructure</subject><subject>Confocal microscopy</subject><subject>Cytometry</subject><subject>Cytotoxicity</subject><subject>DNA microarrays</subject><subject>Dose-Response Relationship, Drug</subject><subject>Electron microscopy</subject><subject>Flow cytometry</subject><subject>garcinielliptone FC</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>HT29 Cells</subject><subject>human colorectal cancer</subject><subject>Humans</subject><subject>Inhibitors</subject><subject>Membrane vesicles</subject><subject>Organelles</subject><subject>Phagocytosis</subject><subject>Phosphatidylinositol 3-Kinase - metabolism</subject><subject>Polyphenols</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Ribosomal Protein S6 Kinases, 70-kDa - metabolism</subject><subject>RNA Interference</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Time Factors</subject><subject>TOR protein</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><subject>Toxicity</subject><subject>Transfection</subject><subject>Transmission electron microscopy</subject><subject>Triterpenes - pharmacology</subject><subject>Tumor cell lines</subject><issn>0021-9541</issn><issn>1097-4652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kD1PwzAQhi0EoqUw8AeQJSaGtHacL49VRPlQJRhgjhzn0rpK42A7Kvn3GFLYmO6ke-493YPQNSVzSki42MluHsackhM0pYSnQZTE4Sma-hkNeBzRCbqwdkcI4ZyxczQJs5BHjIVTJJa9091WbAa8h0oJBxbLwWmnP5VUbsC6xtt-L1osdaMNSCcaLEUrwWAJTWOxM-C3KnxQbos3wkjVKj9QndMt4FV-ic5q0Vi4OtYZel_dv-WPwfrl4SlfrgPJYkaCMoqTOCoZr2jGaZKAFDJk4Js6FGUi6yRjaUkF0DqNGMiKRkBZKrMyqeK0JGyGbsfczuiPHqwrdro3rT9ZUP8sZRFJE0_djZQ02loDddEZtRdmKCgpvmUWXmbxI9OzN8fEvvRy_shfex5YjMBBNTD8n1Q8569j5BeioH8z</recordid><startdate>201801</startdate><enddate>201801</enddate><creator>Won, Shen‐Jeu</creator><creator>Yen, Cheng‐Hsin</creator><creator>Lin, Ting‐Yu</creator><creator>Jiang‐Shieh, Ya‐Fen</creator><creator>Lin, Chun‐Nan</creator><creator>Chen, Jyun‐Ti</creator><creator>Su, Chun‐Li</creator><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>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><orcidid>https://orcid.org/0000-0001-7617-2077</orcidid></search><sort><creationdate>201801</creationdate><title>Autophagy mediates cytotoxicity of human colorectal cancer cells treated with garcinielliptone FC</title><author>Won, Shen‐Jeu ; Yen, Cheng‐Hsin ; Lin, Ting‐Yu ; Jiang‐Shieh, Ya‐Fen ; Lin, Chun‐Nan ; Chen, Jyun‐Ti ; Su, Chun‐Li</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3530-b45654b39d189166ecac23e66ef2ab6cf6837b1ae1f743ecd14e137c8b6d57b03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Antineoplastic Agents, Phytogenic - pharmacology</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Autophagy</topic><topic>Autophagy - drug effects</topic><topic>Autophagy-Related Protein 12 - genetics</topic><topic>Autophagy-Related Protein 12 - metabolism</topic><topic>Autophagy-Related Protein 5 - genetics</topic><topic>Autophagy-Related Protein 5 - metabolism</topic><topic>Beclin-1 - genetics</topic><topic>Beclin-1 - metabolism</topic><topic>Cancer</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Colorectal Neoplasms - drug therapy</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - metabolism</topic><topic>Colorectal Neoplasms - ultrastructure</topic><topic>Confocal microscopy</topic><topic>Cytometry</topic><topic>Cytotoxicity</topic><topic>DNA microarrays</topic><topic>Dose-Response Relationship, Drug</topic><topic>Electron microscopy</topic><topic>Flow cytometry</topic><topic>garcinielliptone FC</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes</topic><topic>HT29 Cells</topic><topic>human colorectal cancer</topic><topic>Humans</topic><topic>Inhibitors</topic><topic>Membrane vesicles</topic><topic>Organelles</topic><topic>Phagocytosis</topic><topic>Phosphatidylinositol 3-Kinase - metabolism</topic><topic>Polyphenols</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Ribosomal Protein S6 Kinases, 70-kDa - metabolism</topic><topic>RNA Interference</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Time Factors</topic><topic>TOR protein</topic><topic>TOR Serine-Threonine Kinases - metabolism</topic><topic>Toxicity</topic><topic>Transfection</topic><topic>Transmission electron microscopy</topic><topic>Triterpenes - pharmacology</topic><topic>Tumor cell lines</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Won, Shen‐Jeu</creatorcontrib><creatorcontrib>Yen, Cheng‐Hsin</creatorcontrib><creatorcontrib>Lin, Ting‐Yu</creatorcontrib><creatorcontrib>Jiang‐Shieh, Ya‐Fen</creatorcontrib><creatorcontrib>Lin, Chun‐Nan</creatorcontrib><creatorcontrib>Chen, Jyun‐Ti</creatorcontrib><creatorcontrib>Su, Chun‐Li</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Journal of cellular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Won, Shen‐Jeu</au><au>Yen, Cheng‐Hsin</au><au>Lin, Ting‐Yu</au><au>Jiang‐Shieh, Ya‐Fen</au><au>Lin, Chun‐Nan</au><au>Chen, Jyun‐Ti</au><au>Su, Chun‐Li</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Autophagy mediates cytotoxicity of human colorectal cancer cells treated with garcinielliptone FC</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J Cell Physiol</addtitle><date>2018-01</date><risdate>2018</risdate><volume>233</volume><issue>1</issue><spage>497</spage><epage>505</epage><pages>497-505</pages><issn>0021-9541</issn><eissn>1097-4652</eissn><abstract>The tautomeric pair of garcinielliptone FC (GFC) is a novel tautomeric pair of polyprenyl benzophenonoid isolated from the pericarps of Garcinia subelliptica Merr. (G. subelliptica, Clusiaceae), a tree with abundant sources of polyphenols. Our previous report demonstrated that GFC induced apoptosis on various types of human cancer cell lines including chemoresistant human colorectal cancer HT‐29 cells. In the present study, we observed that many autophagy‐related genes in GFC‐treated HT‐29 cells were up‐ and down‐regulated using a cDNA microarray containing oncogenes and kinase genes. GFC‐induced autophagy of HT‐29 cells was confirmed by observing the formation of acidic vesicular organelles, LC3 puncta, and double‐membrane autophagic vesicles using flow cytometry, confocal microscopy, and transmission electron microscopy, respectively. Inhibition of AKT/mTOR/P70S6K signaling as well as formation of Atg5‐Atg12 and PI3K/Beclin‐1 complexes were observed using Western blot. Administration of autophagy inhibitor (3‐methyladenine and shRNA Atg5) and apoptosis inhibitor Z‐VAD showed that the GFC‐induced autophagy was cytotoxic form and GFC‐induced apoptosis enhanced GFC‐induced autophagy. Our data suggest the involvement of autophagy and apoptosis in GFC‐induced anticancer mechanisms of human colorectal cancer.
The tautomeric pair of garcinielliptone FC (GFC) is a novel tautomeric pair of polyprenyl benzophenonoid isolated from the pericarps of Garcinia subelliptica Merr. (G. subelliptica, Clusiaceae), a tree with abundant sources of polyphenols. GFC‐induced autophagy was cytotoxic form and GFC‐induced apoptosis enhanced GFC‐induced autophagy.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>28294332</pmid><doi>10.1002/jcp.25910</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0001-7617-2077</orcidid></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Antineoplastic Agents, Phytogenic - pharmacology Apoptosis Apoptosis - drug effects Autophagy Autophagy - drug effects Autophagy-Related Protein 12 - genetics Autophagy-Related Protein 12 - metabolism Autophagy-Related Protein 5 - genetics Autophagy-Related Protein 5 - metabolism Beclin-1 - genetics Beclin-1 - metabolism Cancer Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - drug therapy Colorectal Neoplasms - genetics Colorectal Neoplasms - metabolism Colorectal Neoplasms - ultrastructure Confocal microscopy Cytometry Cytotoxicity DNA microarrays Dose-Response Relationship, Drug Electron microscopy Flow cytometry garcinielliptone FC Gene Expression Regulation, Neoplastic Genes HT29 Cells human colorectal cancer Humans Inhibitors Membrane vesicles Organelles Phagocytosis Phosphatidylinositol 3-Kinase - metabolism Polyphenols Proto-Oncogene Proteins c-akt - metabolism Ribosomal Protein S6 Kinases, 70-kDa - metabolism RNA Interference RNA, Messenger - genetics RNA, Messenger - metabolism Signal Transduction - drug effects Time Factors TOR protein TOR Serine-Threonine Kinases - metabolism Toxicity Transfection Transmission electron microscopy Triterpenes - pharmacology Tumor cell lines |
| title | Autophagy mediates cytotoxicity of human colorectal cancer cells treated with garcinielliptone FC |
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