Acovenoside A Induces Mitotic Catastrophe Followed by Apoptosis in Non-Small-Cell Lung Cancer Cells

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dc.AffiliationOctober University for modern sciences and Arts (MSA)
dc.contributor.authorEl Gaafary M.
dc.contributor.authorEzzat, Shahira M
dc.contributor.authorEl Sayed A.M.
dc.contributor.authorSabry O.M.
dc.contributor.authorHafner S.
dc.contributor.authorLang S.
dc.contributor.authorSchmiech M.
dc.contributor.authorSyrovets T.
dc.contributor.authorSimmet T.
dc.contributor.otherDepartment of Pharmacognosy
dc.contributor.otherCollege of Pharmacy
dc.contributor.otherCairo University
dc.contributor.otherGiza
dc.contributor.other11562
dc.contributor.otherEgypt; Pharmacognosy Department
dc.contributor.otherFaculty of Pharmacy
dc.contributor.otherOctober University for Modern Sciences and Arts (MSA)
dc.contributor.otherCairo
dc.contributor.other11562
dc.contributor.otherEgypt; Institute of Pharmacology of Natural Products and Clinical Pharmacology
dc.contributor.otherUlm University
dc.contributor.otherUlm
dc.contributor.otherD-89081
dc.contributor.otherGermany
dc.date.accessioned2020-01-09T20:41:10Z
dc.date.available2020-01-09T20:41:10Z
dc.date.issued2017
dc.descriptionScopus
dc.description.abstractWe investigated the cytotoxic potential of the cardenolide glycoside acovenoside A against non-small-cell lung cancer cells. Lung cancer is the leading cause of cancer-related mortality and the second most common cancer diagnosed. Epidemiological studies revealed a direct correlation between the regular administration of cardiac glycosides and a lower incidence of various cancers. Acovenoside A, isolated from the pericarps of Acokanthera oppositifolia, potently inhibited proliferation and induced cytotoxicity in A549 non-small-cell lung cancer cells with an IC 50 of 68 � 3 nM after 48 h of exposure. Compared to the antineoplastic agent doxorubicin, acovenoside A was more potent in inhibiting the viability of A549 cancer cells. Moreover, acovenoside A exhibited selectivity against cancer cells, being significantly less toxic to lung fibroblasts and nontoxic for peripheral blood mononuclear cells. Analysis of the cell cycle profile in acovenoside A-treated A549 cells revealed mitotic arrest, due to accumulation of the G 2 /M regulators cyclin B 1 and CDK1, and cytokinesis failure. Furthermore, acovenoside A affected the mitochondrial membrane integrity and induced production of radical oxygen species, which resulted in induction of canonical apoptosis, manifested by caspase 3 activation and DNA fragmentation. Based on our results, acovenoside A warrants further exploration as a potential anticancer lead. � 2017 The American Chemical Society and American Society of Pharmacognosy.en_US
dc.description.urihttps://www.scimagojr.com/journalsearch.php?q=23053&tip=sid&clean=0
dc.identifier.doihttps://doi.org/10.1021/acs.jnatprod.7b00546
dc.identifier.doiPubMed ID 29190084
dc.identifier.issn1633864
dc.identifier.otherhttps://doi.org/10.1021/acs.jnatprod.7b00546
dc.identifier.otherPubMed ID 29190084
dc.identifier.urihttps://t.ly/LXMeG
dc.language.isoEnglishen_US
dc.publisherAmerican Chemical Societyen_US
dc.relation.ispartofseriesJournal of Natural Products
dc.relation.ispartofseries80
dc.subjectOctober University for Modern Sciences and Arts
dc.subjectجامعة أكتوبر للعلوم الحديثة والآداب
dc.subjectUniversity of Modern Sciences and Arts
dc.subjectMSA University
dc.subjectacovenoside aen_US
dc.subjectcardenolideen_US
dc.subjectcaspase 3en_US
dc.subjectcyclin B1en_US
dc.subjectcyclin dependent kinase 1en_US
dc.subjectcytotoxic agenten_US
dc.subjectdoxorubicinen_US
dc.subjectebselenen_US
dc.subjectnorphenazoneen_US
dc.subjectprotein p53en_US
dc.subjectreactive oxygen metaboliteen_US
dc.subjecttempolen_US
dc.subjectunclassified drugen_US
dc.subjectacovenoside Aen_US
dc.subjectantineoplastic agenten_US
dc.subjectcardenolideen_US
dc.subjectdoxorubicinen_US
dc.subjectreactive oxygen metaboliteen_US
dc.subjectAcokanthera oppositifoliaen_US
dc.subjectapoptosisen_US
dc.subjectArticleen_US
dc.subjectcell cycleen_US
dc.subjectcell cycle progressionen_US
dc.subjectcell proliferationen_US
dc.subjectcell viabilityen_US
dc.subjectcontrolled studyen_US
dc.subjectcytokinesisen_US
dc.subjectcytotoxicityen_US
dc.subjectDNA fragmentationen_US
dc.subjectdrug mechanismen_US
dc.subjectdrug sensitivityen_US
dc.subjectfluorescenceen_US
dc.subjectG2 phase cell cycle checkpointen_US
dc.subjecthumanen_US
dc.subjecthuman cellen_US
dc.subjectIC50en_US
dc.subjectlung fibroblasten_US
dc.subjectlung non-small cell carcinoma cell lineen_US
dc.subjectM phase cell cycle checkpointen_US
dc.subjectmitochondrial membrane potentialen_US
dc.subjectmitosisen_US
dc.subjectmitosis inhibitionen_US
dc.subjectnon small cell lung canceren_US
dc.subjectoxidative stressen_US
dc.subjectpericarpen_US
dc.subjectperipheral blood mononuclear cellen_US
dc.subjectprotein phosphorylationen_US
dc.subjectshruben_US
dc.subjectA-549 cell lineen_US
dc.subjectapoptosisen_US
dc.subjectcell survivalen_US
dc.subjectdrug effecten_US
dc.subjectepidemiologyen_US
dc.subjectfibroblasten_US
dc.subjectlung tumoren_US
dc.subjectmetabolismen_US
dc.subjectmitochondrial membraneen_US
dc.subjectmitosisen_US
dc.subjectmononuclear cellen_US
dc.subjectnon small cell lung canceren_US
dc.subjecttumor cell lineen_US
dc.subjectA549 Cellsen_US
dc.subjectAntineoplastic Agentsen_US
dc.subjectApoptosisen_US
dc.subjectCarcinoma, Non-Small-Cell Lungen_US
dc.subjectCardenolidesen_US
dc.subjectCell Line, Tumoren_US
dc.subjectCell Proliferationen_US
dc.subjectCell Survivalen_US
dc.subjectDNA Fragmentationen_US
dc.subjectDoxorubicinen_US
dc.subjectEpidemiologic Studiesen_US
dc.subjectFibroblastsen_US
dc.subjectG2 Phase Cell Cycle Checkpointsen_US
dc.subjectHumansen_US
dc.subjectLeukocytes, Mononuclearen_US
dc.subjectLung Neoplasmsen_US
dc.subjectMitochondrial Membranesen_US
dc.subjectMitosisen_US
dc.subjectReactive Oxygen Speciesen_US
dc.titleAcovenoside A Induces Mitotic Catastrophe Followed by Apoptosis in Non-Small-Cell Lung Cancer Cellsen_US
dc.typeArticleen_US
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