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Conference Paper: Activation of Pparγ and Inhibition of Xiap in Human Cancer Cells: Synergistic Effects On Cell Proliferation, Apoptosis, and Tumorigenesis

TitleActivation of Pparγ and Inhibition of Xiap in Human Cancer Cells: Synergistic Effects On Cell Proliferation, Apoptosis, and Tumorigenesis
Authors
Issue Date2007
PublisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/gastro
Citation
Digestive Disease Week and the 108th Annual Meeting of the American Gastroenterological Association Institute, Washington, DC, 19-24 May 2007. In Gastroenterology, 2007, v. 132 n. 4, p. A-425 Abstract no. M1973 How to Cite?
AbstractBackground and objectives: In colon cancer, the anti-tumor effect of Peroxisome proliferatoractivated receptor gamma (PPARγ) on tumorigenesis is controversial. Over-expression of Xlinked inhibitor of apoptosis (XIAP) in colon cancer has been linked to treatment resistance and poor prognosis. The aims of our present study are to explore the synergistic effects of PPARγ activation and XIAP inhibition on the cell proliferation, apoptosis, and tumorigenesis in colon cancer In Vitro and In Vivo. Materials and methods: Colon cancer cell line HCT116 XIAP+/+ and HCT116XIAP-/- were cultured, and troglitazone (TGZ) was used as PPARγ agonist. Cell proliferation was measured by WST-1 assay. Apoptosis was determined by ELISA kit. Protein expression was detected by Western blot. In In Vivo tumorigenesis studies, Balb/c nude mice were subcutaneously inoculated with 1×107 cells to generate colon cancer xenograft. TGZ (200 ppm) was given on the day of tumor cell inoculation. The volume of tumor was measured every other day. Expressions of Ki67 and VEGF in tumor tissues were detected by Western blot. Results: TGZ induced apoptosis and inhibited the proliferation of HCT116XIAP+/+ and HCT116XIAP-/- cells in a time- and dose-dependent manner, and these effects were more significant in HCT116XIAP-/- cells. The IC50 values of TGZ against HCT116XIAP+/+ and HCT116XIAP-/- cells after 48h treatment were 88.80μM and 68.04μM, respectively. Caspase 3, 7, 8, and 9, as well as poly(ADP-ribose) polymerase were activated more obviously in HCT116XIAP-/- cells compared to HCT116XIAP+/+ cells. In addition, combined with XIAP inhibitor 1396-12 increased apoptosis and cell growth inhibition in HCT116XIAP+/+ cells when compared to TGZ alone. The study In Vivo showed there was no difference in the tumor development in HCT116XIAP+/+ and HCT116XIAP-/- cells xenograft model. TGZ retarded the growth of xenograft colon cancer, and such a growth inhibition was more significant in HCT116XIAP-/- cells-derived tumors than in HCT116XIAP+/+ cellsderived tumors, with a tumor volume reduction rate of 83.3% and 32.5% on day 33, respectively. This increased therapeutic benefit correlated with significant decreased expression of Ki67 and VEGF in tumors. Conclusion: Simultaneous activation of PPARγ and inhibition of XIAP may have synergistic anti-tumor effect against colon cancer.
Persistent Identifierhttp://hdl.handle.net/10722/102517
ISSN
2015 Impact Factor: 18.187
2015 SCImago Journal Rankings: 7.170

 

DC FieldValueLanguage
dc.contributor.authorDai, Yen_HK
dc.contributor.authorQiao, Len_HK
dc.contributor.authorGu, Qen_HK
dc.contributor.authorXia, HHXen_HK
dc.contributor.authorCheung, TKen_HK
dc.contributor.authorMa, Jen_HK
dc.contributor.authorZou, Ben_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2010-09-25T20:33:51Z-
dc.date.available2010-09-25T20:33:51Z-
dc.date.issued2007en_HK
dc.identifier.citationDigestive Disease Week and the 108th Annual Meeting of the American Gastroenterological Association Institute, Washington, DC, 19-24 May 2007. In Gastroenterology, 2007, v. 132 n. 4, p. A-425 Abstract no. M1973en_HK
dc.identifier.issn0016-5085en_HK
dc.identifier.urihttp://hdl.handle.net/10722/102517-
dc.description.abstractBackground and objectives: In colon cancer, the anti-tumor effect of Peroxisome proliferatoractivated receptor gamma (PPARγ) on tumorigenesis is controversial. Over-expression of Xlinked inhibitor of apoptosis (XIAP) in colon cancer has been linked to treatment resistance and poor prognosis. The aims of our present study are to explore the synergistic effects of PPARγ activation and XIAP inhibition on the cell proliferation, apoptosis, and tumorigenesis in colon cancer In Vitro and In Vivo. Materials and methods: Colon cancer cell line HCT116 XIAP+/+ and HCT116XIAP-/- were cultured, and troglitazone (TGZ) was used as PPARγ agonist. Cell proliferation was measured by WST-1 assay. Apoptosis was determined by ELISA kit. Protein expression was detected by Western blot. In In Vivo tumorigenesis studies, Balb/c nude mice were subcutaneously inoculated with 1×107 cells to generate colon cancer xenograft. TGZ (200 ppm) was given on the day of tumor cell inoculation. The volume of tumor was measured every other day. Expressions of Ki67 and VEGF in tumor tissues were detected by Western blot. Results: TGZ induced apoptosis and inhibited the proliferation of HCT116XIAP+/+ and HCT116XIAP-/- cells in a time- and dose-dependent manner, and these effects were more significant in HCT116XIAP-/- cells. The IC50 values of TGZ against HCT116XIAP+/+ and HCT116XIAP-/- cells after 48h treatment were 88.80μM and 68.04μM, respectively. Caspase 3, 7, 8, and 9, as well as poly(ADP-ribose) polymerase were activated more obviously in HCT116XIAP-/- cells compared to HCT116XIAP+/+ cells. In addition, combined with XIAP inhibitor 1396-12 increased apoptosis and cell growth inhibition in HCT116XIAP+/+ cells when compared to TGZ alone. The study In Vivo showed there was no difference in the tumor development in HCT116XIAP+/+ and HCT116XIAP-/- cells xenograft model. TGZ retarded the growth of xenograft colon cancer, and such a growth inhibition was more significant in HCT116XIAP-/- cells-derived tumors than in HCT116XIAP+/+ cellsderived tumors, with a tumor volume reduction rate of 83.3% and 32.5% on day 33, respectively. This increased therapeutic benefit correlated with significant decreased expression of Ki67 and VEGF in tumors. Conclusion: Simultaneous activation of PPARγ and inhibition of XIAP may have synergistic anti-tumor effect against colon cancer.-
dc.languageengen_HK
dc.publisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/gastroen_HK
dc.relation.ispartofGastroenterologyen_HK
dc.titleActivation of Pparγ and Inhibition of Xiap in Human Cancer Cells: Synergistic Effects On Cell Proliferation, Apoptosis, and Tumorigenesisen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0016-5085&volume=132&issue=4&spage=A425&epage=&date=2007&atitle=Activation+of+Pparc+and+inhibition+of+Xiap+in+human+cancer+cells:+Synergistic+effects+on+cell+proliferation,+apoptosis,+and+tumorigensis.++Digestive+Disease+Week+2007,+Washington+DC,+USA,+19-24+Mayen_HK
dc.identifier.emailDai, Y: daiyun1@medmail.com.cnen_HK
dc.identifier.emailQiao, L: lq8688@hotmail.comen_HK
dc.identifier.emailGu, Q: qingappl@hotmail.comen_HK
dc.identifier.emailXia, HHX: xiaharry@hotmail.comen_HK
dc.identifier.emailCheung, TK: cheungtingkin@yahoo.comen_HK
dc.identifier.emailMa, J: majuan00@hkucc.hku.hken_HK
dc.identifier.emailZou, B: zoubing@hkucc.hku.hken_HK
dc.identifier.emailWong, BCY: bcywong@hku.hken_HK
dc.identifier.authorityQiao, L=rp00513en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0016-5085(07)60009-2-
dc.identifier.hkuros131423en_HK
dc.identifier.volume132en_HK
dc.identifier.issue4en_HK
dc.identifier.spage425en_HK

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