A Dihydroxy-pentamethoxyflavone from Gardenia obtusifolia Suppresses Proliferation and Promotes Apoptosis of Tumor Cells Through Modulation of Multiple Cell Signaling Pathways
Identifieur interne : 000A82 ( Pmc/Curation ); précédent : 000A81; suivant : 000A83A Dihydroxy-pentamethoxyflavone from Gardenia obtusifolia Suppresses Proliferation and Promotes Apoptosis of Tumor Cells Through Modulation of Multiple Cell Signaling Pathways
Auteurs : Kanokkarn Phromnoi [États-Unis, Thaïlande] ; Simone Reuter [États-Unis] ; Bokyung Sung [États-Unis] ; Pornngarm Limtrakul [Thaïlande] ; Bharat B. Aggarwal [États-Unis]Source :
- Anticancer research [ 0250-7005 ] ; 2010.
Abstract
We sought to determine the molecular basis for the anticancer activities of 5,3′-dihydroxy-3,6,7,8,4′-pentamethoxyflavone (DH-PMF), isolated from Gardenia obtusifolia traditionally used in Thailand for a variety of ailments. As little as 1 μM DH-PMF inhibited the proliferation of prostate, colon, kidney, lung, head and neck, pancreas, breast, leukemia, and myeloma cancer cell lines. DH-PMF also suppressed the colony-forming ability of tumor cells, with 50% inhibition occurring at a dose less than 10 nM. DH-PMF induced G2/M and subG1 cell cycle arrest, increased the levels of p21WAF1/CIP1 and p27KIP1, and reduced the expression of cyclin D1, CDC2, and c-MYC. Furthermore, DH-PMF inhibited AKT and glycogen synthase kinase 3 beta (GSK3β) activation, reduced cell survival proteins, and induced apoptosis, as indicated by annexin V staining, TUNEL assay, and activation of caspase-8, -9 and -3. Overall, our results demonstrate that DH-PMF induces suppression of cell proliferation through modulation of AKT-GSK3β pathways and induction of cyclin-dependent kinase (CDK) inhibitors.
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PubMed: 20944143
PubMed Central: 3142747
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">A Dihydroxy-pentamethoxyflavone from <italic>Gardenia obtusifolia</italic> Suppresses Proliferation and Promotes Apoptosis of Tumor Cells Through Modulation of Multiple Cell Signaling Pathways</title><author><name sortKey="Phromnoi, Kanokkarn" sort="Phromnoi, Kanokkarn" uniqKey="Phromnoi K" first="Kanokkarn" last="Phromnoi">Kanokkarn Phromnoi</name><affiliation wicri:level="1"><nlm:aff id="A1"> Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, U.S.A</nlm:aff><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea> Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="A2"> Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand</nlm:aff><country xml:lang="fr">Thaïlande</country><wicri:regionArea> Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai</wicri:regionArea></affiliation></author><author><name sortKey="Reuter, Simone" sort="Reuter, Simone" uniqKey="Reuter S" first="Simone" last="Reuter">Simone Reuter</name><affiliation wicri:level="1"><nlm:aff id="A1"> Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, U.S.A</nlm:aff><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea> Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas</wicri:regionArea></affiliation></author><author><name sortKey="Sung, Bokyung" sort="Sung, Bokyung" uniqKey="Sung B" first="Bokyung" last="Sung">Bokyung Sung</name><affiliation wicri:level="1"><nlm:aff id="A1"> Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, U.S.A</nlm:aff><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea> Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas</wicri:regionArea></affiliation></author><author><name sortKey="Limtrakul, Pornngarm" sort="Limtrakul, Pornngarm" uniqKey="Limtrakul P" first="Pornngarm" last="Limtrakul">Pornngarm Limtrakul</name><affiliation wicri:level="1"><nlm:aff id="A2"> Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand</nlm:aff><country xml:lang="fr">Thaïlande</country><wicri:regionArea> Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai</wicri:regionArea></affiliation></author><author><name sortKey="Aggarwal, Bharat B" sort="Aggarwal, Bharat B" uniqKey="Aggarwal B" first="Bharat B." last="Aggarwal">Bharat B. Aggarwal</name><affiliation wicri:level="1"><nlm:aff id="A1"> Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, U.S.A</nlm:aff><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea> Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">20944143</idno><idno type="pmc">3142747</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3142747</idno><idno type="RBID">PMC:3142747</idno><date when="2010">2010</date><idno type="wicri:Area/Pmc/Corpus">000A83</idno><idno type="wicri:Area/Pmc/Curation">000A82</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">A Dihydroxy-pentamethoxyflavone from <italic>Gardenia obtusifolia</italic> Suppresses Proliferation and Promotes Apoptosis of Tumor Cells Through Modulation of Multiple Cell Signaling Pathways</title><author><name sortKey="Phromnoi, Kanokkarn" sort="Phromnoi, Kanokkarn" uniqKey="Phromnoi K" first="Kanokkarn" last="Phromnoi">Kanokkarn Phromnoi</name><affiliation wicri:level="1"><nlm:aff id="A1"> Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, U.S.A</nlm:aff><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea> Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="A2"> Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand</nlm:aff><country xml:lang="fr">Thaïlande</country><wicri:regionArea> Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai</wicri:regionArea></affiliation></author><author><name sortKey="Reuter, Simone" sort="Reuter, Simone" uniqKey="Reuter S" first="Simone" last="Reuter">Simone Reuter</name><affiliation wicri:level="1"><nlm:aff id="A1"> Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, U.S.A</nlm:aff><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea> Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas</wicri:regionArea></affiliation></author><author><name sortKey="Sung, Bokyung" sort="Sung, Bokyung" uniqKey="Sung B" first="Bokyung" last="Sung">Bokyung Sung</name><affiliation wicri:level="1"><nlm:aff id="A1"> Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, U.S.A</nlm:aff><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea> Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas</wicri:regionArea></affiliation></author><author><name sortKey="Limtrakul, Pornngarm" sort="Limtrakul, Pornngarm" uniqKey="Limtrakul P" first="Pornngarm" last="Limtrakul">Pornngarm Limtrakul</name><affiliation wicri:level="1"><nlm:aff id="A2"> Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand</nlm:aff><country xml:lang="fr">Thaïlande</country><wicri:regionArea> Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai</wicri:regionArea></affiliation></author><author><name sortKey="Aggarwal, Bharat B" sort="Aggarwal, Bharat B" uniqKey="Aggarwal B" first="Bharat B." last="Aggarwal">Bharat B. Aggarwal</name><affiliation wicri:level="1"><nlm:aff id="A1"> Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, U.S.A</nlm:aff><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea> Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas</wicri:regionArea></affiliation></author></analytic><series><title level="j">Anticancer research</title><idno type="ISSN">0250-7005</idno><idno type="eISSN">1791-7530</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">We sought to determine the molecular basis for the anticancer activities of 5,3′-dihydroxy-3,6,7,8,4′-pentamethoxyflavone (DH-PMF), isolated from Gardenia obtusifolia traditionally used in Thailand for a variety of ailments. As little as 1 μM DH-PMF inhibited the proliferation of prostate, colon, kidney, lung, head and neck, pancreas, breast, leukemia, and myeloma cancer cell lines. DH-PMF also suppressed the colony-forming ability of tumor cells, with 50% inhibition occurring at a dose less than 10 nM. DH-PMF induced G<sub>2</sub>/M and subG<sub>1</sub> cell cycle arrest, increased the levels of p21<sup>WAF1/CIP1</sup> and p27<sup>KIP1</sup>, and reduced the expression of cyclin D1, CDC2, and c-MYC. Furthermore, DH-PMF inhibited AKT and glycogen synthase kinase 3 beta (GSK3β) activation, reduced cell survival proteins, and induced apoptosis, as indicated by annexin V staining, TUNEL assay, and activation of caspase-8, -9 and -3. Overall, our results demonstrate that DH-PMF induces suppression of cell proliferation through modulation of AKT-GSK3β pathways and induction of cyclin-dependent kinase (CDK) inhibitors.</p></div></front></TEI><pmc article-type="research-article" xml:lang="en"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">8102988</journal-id><journal-id journal-id-type="pubmed-jr-id">592</journal-id><journal-id journal-id-type="nlm-ta">Anticancer Res</journal-id><journal-title-group><journal-title>Anticancer research</journal-title></journal-title-group><issn pub-type="ppub">0250-7005</issn><issn pub-type="epub">1791-7530</issn></journal-meta><article-meta><article-id pub-id-type="pmid">20944143</article-id><article-id pub-id-type="pmc">3142747</article-id><article-id pub-id-type="manuscript">NIHMS307526</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>A Dihydroxy-pentamethoxyflavone from <italic>Gardenia obtusifolia</italic> Suppresses Proliferation and Promotes Apoptosis of Tumor Cells Through Modulation of Multiple Cell Signaling Pathways</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>PHROMNOI</surname><given-names>KANOKKARN</given-names></name><xref rid="A1" ref-type="aff">1</xref><xref rid="A2" ref-type="aff">2</xref></contrib><contrib contrib-type="author"><name><surname>REUTER</surname><given-names>SIMONE</given-names></name><xref rid="A1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>SUNG</surname><given-names>BOKYUNG</given-names></name><xref rid="A1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>LIMTRAKUL</surname><given-names>PORNNGARM</given-names></name><xref rid="A2" ref-type="aff">2</xref></contrib><contrib contrib-type="author"><name><surname>AGGARWAL</surname><given-names>BHARAT B.</given-names></name><xref rid="A1" ref-type="aff">1</xref></contrib></contrib-group><aff id="A1"><label>1</label> Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, U.S.A</aff><aff id="A2"><label>2</label> Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand</aff><author-notes><corresp id="FN1">Correspondence to: Bharat B. Aggarwal, Ph.D., Department of Experimental Therapeutics, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Box 143, Houston, TX 77030, U.S.A. Tel: +1 7137941817, Fax: +1 7137456339, <email>aggarwal@mdanderson.org</email> and Pornngarm Limtrakul, Ph.D., Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand. Tel: +66 053945323, Fax: +66 053894031, <email>plimtrak@mail.med.cmu.ac.th</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>6</day><month>7</month><year>2011</year></pub-date><pub-date pub-type="ppub"><month>9</month><year>2010</year></pub-date><pub-date pub-type="pmc-release"><day>25</day><month>7</month><year>2011</year></pub-date><volume>30</volume><issue>9</issue><fpage>3599</fpage><lpage>3610</lpage><abstract><p id="P1">We sought to determine the molecular basis for the anticancer activities of 5,3′-dihydroxy-3,6,7,8,4′-pentamethoxyflavone (DH-PMF), isolated from Gardenia obtusifolia traditionally used in Thailand for a variety of ailments. As little as 1 μM DH-PMF inhibited the proliferation of prostate, colon, kidney, lung, head and neck, pancreas, breast, leukemia, and myeloma cancer cell lines. DH-PMF also suppressed the colony-forming ability of tumor cells, with 50% inhibition occurring at a dose less than 10 nM. DH-PMF induced G<sub>2</sub>/M and subG<sub>1</sub> cell cycle arrest, increased the levels of p21<sup>WAF1/CIP1</sup> and p27<sup>KIP1</sup>, and reduced the expression of cyclin D1, CDC2, and c-MYC. Furthermore, DH-PMF inhibited AKT and glycogen synthase kinase 3 beta (GSK3β) activation, reduced cell survival proteins, and induced apoptosis, as indicated by annexin V staining, TUNEL assay, and activation of caspase-8, -9 and -3. Overall, our results demonstrate that DH-PMF induces suppression of cell proliferation through modulation of AKT-GSK3β pathways and induction of cyclin-dependent kinase (CDK) inhibitors.</p></abstract><kwd-group><kwd>AKT</kwd><kwd>GSK3beta</kwd><kwd>natural products</kwd><kwd>plant extract</kwd><kwd>CDK inhibitor</kwd></kwd-group><funding-group><award-group><funding-source country="United States">National Cancer Institute : NCI</funding-source><award-id>P01 CA124787-01A2 || CA</award-id></award-group></funding-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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