Cistanche tubulosa phenylethanoid glycosides induce apoptosis in Eca-109 cells via the mitochondria-dependent pathway
has various biological functions. In the present study, the antitumor effect of water-soluble phenylethanoid glycosides of . (CTPG-W) on esophageal cancer was investigated. Eca-109 cells were treated with CTPG-W and the cell viability was measured by MTT assay. The apoptosis, cell cycle, mitochondri...
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Veröffentlicht in: | Oncology letters 2019-01, Vol.17 (1), p.303-313 |
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creator | Fu, Changshuang Li, Jinyu Aipire, Adila Xia, Lijie Yang, Yi Chen, Qiuyan Lv, Jie Wang, Xinhui Li, Jinyao |
description | has various biological functions. In the present study, the antitumor effect of water-soluble phenylethanoid glycosides of
.
(CTPG-W) on esophageal cancer was investigated. Eca-109 cells were treated with CTPG-W and the cell viability was measured by MTT assay. The apoptosis, cell cycle, mitochondrial membrane potential (Δψm) and reactive oxygen species were analyzed by flow cytometry. The levels of proteins in apoptotic pathways were detected by western blot analysis. It was determined that CTPG-W significantly reduced the viability of Eca-109 cells through the induction of apoptosis and cell cycle arrest. Following CTPG-W treatment, the Δψm of Eca-109 was notably decreased, which is associated with the upregulated levels of B-cell lymphoma-2 (Bcl-2)-associated X and downregulated levels of Bcl-2. Consequently, the levels of cytochrome
and c-Jun NH
-terminal kinase were increased, which upregulated the levels of cleaved-poly (ADP-ribose) polymerase and cleaved-caspase-3, -7 and -9, but not caspase-8. Correspondingly, the levels of reactive oxygen species in Eca-109 cells demonstrated notable changes. These results indicated that CTPG-W induced apoptosis of Eca-109 cells through a mitochondrial-dependent pathway. |
doi_str_mv | 10.3892/ol.2018.9635 |
format | Article |
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.
(CTPG-W) on esophageal cancer was investigated. Eca-109 cells were treated with CTPG-W and the cell viability was measured by MTT assay. The apoptosis, cell cycle, mitochondrial membrane potential (Δψm) and reactive oxygen species were analyzed by flow cytometry. The levels of proteins in apoptotic pathways were detected by western blot analysis. It was determined that CTPG-W significantly reduced the viability of Eca-109 cells through the induction of apoptosis and cell cycle arrest. Following CTPG-W treatment, the Δψm of Eca-109 was notably decreased, which is associated with the upregulated levels of B-cell lymphoma-2 (Bcl-2)-associated X and downregulated levels of Bcl-2. Consequently, the levels of cytochrome
and c-Jun NH
-terminal kinase were increased, which upregulated the levels of cleaved-poly (ADP-ribose) polymerase and cleaved-caspase-3, -7 and -9, but not caspase-8. Correspondingly, the levels of reactive oxygen species in Eca-109 cells demonstrated notable changes. These results indicated that CTPG-W induced apoptosis of Eca-109 cells through a mitochondrial-dependent pathway.</description><identifier>ISSN: 1792-1074</identifier><identifier>EISSN: 1792-1082</identifier><identifier>DOI: 10.3892/ol.2018.9635</identifier><identifier>PMID: 30655768</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Apoptosis ; Cell cycle ; Chemotherapy ; Colorectal cancer ; Cytochromes ; Esophageal cancer ; Genetic aspects ; Herbal medicine ; Laboratory animals ; Liver cancer ; Medical prognosis ; Mitochondria ; Mortality ; Oncology ; Radiation therapy ; Reactive oxygen species ; Studies</subject><ispartof>Oncology letters, 2019-01, Vol.17 (1), p.303-313</ispartof><rights>COPYRIGHT 2019 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2019</rights><rights>Copyright: © Fu et al. 2019</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c510t-54fe59ad2ff9dc86aa488b5dadfc0a6f42b0f62b2bef01578892227e0424c7293</citedby><cites>FETCH-LOGICAL-c510t-54fe59ad2ff9dc86aa488b5dadfc0a6f42b0f62b2bef01578892227e0424c7293</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6313098/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6313098/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30655768$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fu, Changshuang</creatorcontrib><creatorcontrib>Li, Jinyu</creatorcontrib><creatorcontrib>Aipire, Adila</creatorcontrib><creatorcontrib>Xia, Lijie</creatorcontrib><creatorcontrib>Yang, Yi</creatorcontrib><creatorcontrib>Chen, Qiuyan</creatorcontrib><creatorcontrib>Lv, Jie</creatorcontrib><creatorcontrib>Wang, Xinhui</creatorcontrib><creatorcontrib>Li, Jinyao</creatorcontrib><title>Cistanche tubulosa phenylethanoid glycosides induce apoptosis in Eca-109 cells via the mitochondria-dependent pathway</title><title>Oncology letters</title><addtitle>Oncol Lett</addtitle><description>has various biological functions. In the present study, the antitumor effect of water-soluble phenylethanoid glycosides of
.
(CTPG-W) on esophageal cancer was investigated. Eca-109 cells were treated with CTPG-W and the cell viability was measured by MTT assay. The apoptosis, cell cycle, mitochondrial membrane potential (Δψm) and reactive oxygen species were analyzed by flow cytometry. The levels of proteins in apoptotic pathways were detected by western blot analysis. It was determined that CTPG-W significantly reduced the viability of Eca-109 cells through the induction of apoptosis and cell cycle arrest. Following CTPG-W treatment, the Δψm of Eca-109 was notably decreased, which is associated with the upregulated levels of B-cell lymphoma-2 (Bcl-2)-associated X and downregulated levels of Bcl-2. Consequently, the levels of cytochrome
and c-Jun NH
-terminal kinase were increased, which upregulated the levels of cleaved-poly (ADP-ribose) polymerase and cleaved-caspase-3, -7 and -9, but not caspase-8. Correspondingly, the levels of reactive oxygen species in Eca-109 cells demonstrated notable changes. These results indicated that CTPG-W induced apoptosis of Eca-109 cells through a mitochondrial-dependent pathway.</description><subject>Apoptosis</subject><subject>Cell cycle</subject><subject>Chemotherapy</subject><subject>Colorectal cancer</subject><subject>Cytochromes</subject><subject>Esophageal cancer</subject><subject>Genetic aspects</subject><subject>Herbal medicine</subject><subject>Laboratory animals</subject><subject>Liver cancer</subject><subject>Medical prognosis</subject><subject>Mitochondria</subject><subject>Mortality</subject><subject>Oncology</subject><subject>Radiation therapy</subject><subject>Reactive oxygen species</subject><subject>Studies</subject><issn>1792-1074</issn><issn>1792-1082</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkk1v3CAQhq2qVROlufVcWapU9VBvMTYYXypFq_RDitRLe0ZjGNZELLgGJ9p_X6yk22xVOICGZ16YlymK1zXZNKKnH4PbUFKLTc8b9qw4r7ueVjUR9Plx37VnxWWMtyQPxmsh-MvirCGcsY6L82LZ2pjAqxHLtAyLCxHKaUR_cJhG8MHqcucOKkSrMZbW60VhCVOYUg6tgfJaQb6mLxU6F8s7C2XKYnubghqD17OFSuOEXqNP5QRpvIfDq-KFARfx8nG9KH5-vv6x_VrdfP_ybXt1UylWk1Sx1iDrQVNjeq0EB2iFGJgGbRQBblo6EMPpQAc0pGadyJZQ2iFpaas62jcXxacH3WkZ9qhVfsIMTk6z3cN8kAGsPD3xdpS7cCd5UzekF1ng_aPAHH4tGJPc27hWCh7DEiXNLjc8f0WX0bf_oLdhmX0uL1OcdkR0gv6lduBQWm9CvletovKK8T4X0JM2U5v_UHlq3FsVPBqb4ycJ754kjAgujTG4Jdng4yn44QFUc4hxRnM0oyZybSkZnFxbSq4tlfE3Tw08wn8aqPkNWJbHGQ</recordid><startdate>20190101</startdate><enddate>20190101</enddate><creator>Fu, Changshuang</creator><creator>Li, Jinyu</creator><creator>Aipire, Adila</creator><creator>Xia, Lijie</creator><creator>Yang, Yi</creator><creator>Chen, Qiuyan</creator><creator>Lv, Jie</creator><creator>Wang, Xinhui</creator><creator>Li, Jinyao</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20190101</creationdate><title>Cistanche tubulosa phenylethanoid glycosides induce apoptosis in Eca-109 cells via the mitochondria-dependent pathway</title><author>Fu, Changshuang ; Li, Jinyu ; Aipire, Adila ; Xia, Lijie ; Yang, Yi ; Chen, Qiuyan ; Lv, Jie ; Wang, Xinhui ; Li, Jinyao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c510t-54fe59ad2ff9dc86aa488b5dadfc0a6f42b0f62b2bef01578892227e0424c7293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Apoptosis</topic><topic>Cell cycle</topic><topic>Chemotherapy</topic><topic>Colorectal cancer</topic><topic>Cytochromes</topic><topic>Esophageal cancer</topic><topic>Genetic aspects</topic><topic>Herbal medicine</topic><topic>Laboratory animals</topic><topic>Liver cancer</topic><topic>Medical prognosis</topic><topic>Mitochondria</topic><topic>Mortality</topic><topic>Oncology</topic><topic>Radiation therapy</topic><topic>Reactive oxygen species</topic><topic>Studies</topic><toplevel>online_resources</toplevel><creatorcontrib>Fu, Changshuang</creatorcontrib><creatorcontrib>Li, Jinyu</creatorcontrib><creatorcontrib>Aipire, Adila</creatorcontrib><creatorcontrib>Xia, Lijie</creatorcontrib><creatorcontrib>Yang, Yi</creatorcontrib><creatorcontrib>Chen, Qiuyan</creatorcontrib><creatorcontrib>Lv, Jie</creatorcontrib><creatorcontrib>Wang, Xinhui</creatorcontrib><creatorcontrib>Li, Jinyao</creatorcontrib><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>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>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fu, Changshuang</au><au>Li, Jinyu</au><au>Aipire, Adila</au><au>Xia, Lijie</au><au>Yang, Yi</au><au>Chen, Qiuyan</au><au>Lv, Jie</au><au>Wang, Xinhui</au><au>Li, Jinyao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cistanche tubulosa phenylethanoid glycosides induce apoptosis in Eca-109 cells via the mitochondria-dependent pathway</atitle><jtitle>Oncology letters</jtitle><addtitle>Oncol Lett</addtitle><date>2019-01-01</date><risdate>2019</risdate><volume>17</volume><issue>1</issue><spage>303</spage><epage>313</epage><pages>303-313</pages><issn>1792-1074</issn><eissn>1792-1082</eissn><abstract>has various biological functions. In the present study, the antitumor effect of water-soluble phenylethanoid glycosides of
.
(CTPG-W) on esophageal cancer was investigated. Eca-109 cells were treated with CTPG-W and the cell viability was measured by MTT assay. The apoptosis, cell cycle, mitochondrial membrane potential (Δψm) and reactive oxygen species were analyzed by flow cytometry. The levels of proteins in apoptotic pathways were detected by western blot analysis. It was determined that CTPG-W significantly reduced the viability of Eca-109 cells through the induction of apoptosis and cell cycle arrest. Following CTPG-W treatment, the Δψm of Eca-109 was notably decreased, which is associated with the upregulated levels of B-cell lymphoma-2 (Bcl-2)-associated X and downregulated levels of Bcl-2. Consequently, the levels of cytochrome
and c-Jun NH
-terminal kinase were increased, which upregulated the levels of cleaved-poly (ADP-ribose) polymerase and cleaved-caspase-3, -7 and -9, but not caspase-8. Correspondingly, the levels of reactive oxygen species in Eca-109 cells demonstrated notable changes. These results indicated that CTPG-W induced apoptosis of Eca-109 cells through a mitochondrial-dependent pathway.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>30655768</pmid><doi>10.3892/ol.2018.9635</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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source | Spandidos Publications Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
subjects | Apoptosis Cell cycle Chemotherapy Colorectal cancer Cytochromes Esophageal cancer Genetic aspects Herbal medicine Laboratory animals Liver cancer Medical prognosis Mitochondria Mortality Oncology Radiation therapy Reactive oxygen species Studies |
title | Cistanche tubulosa phenylethanoid glycosides induce apoptosis in Eca-109 cells via the mitochondria-dependent pathway |
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