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Article: The role of Id-1 in chemosensitivity and epirubicin-induced apoptosis in bladder cancer cells

TitleThe role of Id-1 in chemosensitivity and epirubicin-induced apoptosis in bladder cancer cells
Authors
KeywordsApoptosis
Bladder Cancer Cells
Chemosensitivity
Epirubicin
Id-1
Issue Date2009
PublisherDemetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/OR/or.htm
Citation
Oncology Reports, 2009, v. 21 n. 4, p. 1053-1059 How to Cite?
AbstractRecurrence and progression are the major problems in the treatment of bladder cancer. Increased expression of Id-1, a basic helix-loop-helix transcription factor, has recently been shown in several types of advanced cancer. Some studies have provided evidence to suggest that Id-1 can be considered a potential therapeutic target. The objective of this study was to investigate the role of Id-1 in the chemosensitivity of bladder cancer cells, and the effect of Id-1 on chemotherapeutic drug-induced apoptosis in bladder cancer cells. We compared the different sensitivity to epirubicin in RT112 and MGH-U1 cell lines with different Id-1 expression. Then, we transfected different vectors into RT112 and MGH-U1 respectively, and generated the stable Id-1 up-regulation and down-regulation transfectants. The results of cell viability assay showed up-regulation of Id-1 in RT112 leading to increased sensitivity in response to epirubicin, and downregulation of Id-1 increased cellular sensitivity to epirubicin. Furthermore, the analysis of apoptosis related protein revealed that up-regulation of Id-1 suppressed epirubicininduced apoptosis and down-regulation of Id-1 leading to increased epirubicin-induced apoptosis. Wound closure assay showed up-regulation of Id-1 leading to improved migration abilities of bladder cancer cells under chemotherapy. Our results suggest that up-regulation of Id-1 in bladder cancer cells lead to increased cell viability in response to epirubicin by its improved anti-apoptotic role, and down-regulation of Id-1 increases cellular sensitivity to epirubicin by increased anticancer drug-induced apoptosis.
Persistent Identifierhttp://hdl.handle.net/10722/149717
ISSN
2014 Impact Factor: 2.301
2013 SCImago Journal Rankings: 0.935
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHu, Hen_US
dc.contributor.authorHan, HYen_US
dc.contributor.authorWang, YLen_US
dc.contributor.authorZhang, XPen_US
dc.contributor.authorChua, CWen_US
dc.contributor.authorWong, YCen_US
dc.contributor.authorWang, XFen_US
dc.contributor.authorLing, MTen_US
dc.contributor.authorXu, KXen_US
dc.date.accessioned2012-06-26T05:57:34Z-
dc.date.available2012-06-26T05:57:34Z-
dc.date.issued2009en_US
dc.identifier.citationOncology Reports, 2009, v. 21 n. 4, p. 1053-1059en_US
dc.identifier.issn1021-335Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/149717-
dc.description.abstractRecurrence and progression are the major problems in the treatment of bladder cancer. Increased expression of Id-1, a basic helix-loop-helix transcription factor, has recently been shown in several types of advanced cancer. Some studies have provided evidence to suggest that Id-1 can be considered a potential therapeutic target. The objective of this study was to investigate the role of Id-1 in the chemosensitivity of bladder cancer cells, and the effect of Id-1 on chemotherapeutic drug-induced apoptosis in bladder cancer cells. We compared the different sensitivity to epirubicin in RT112 and MGH-U1 cell lines with different Id-1 expression. Then, we transfected different vectors into RT112 and MGH-U1 respectively, and generated the stable Id-1 up-regulation and down-regulation transfectants. The results of cell viability assay showed up-regulation of Id-1 in RT112 leading to increased sensitivity in response to epirubicin, and downregulation of Id-1 increased cellular sensitivity to epirubicin. Furthermore, the analysis of apoptosis related protein revealed that up-regulation of Id-1 suppressed epirubicininduced apoptosis and down-regulation of Id-1 leading to increased epirubicin-induced apoptosis. Wound closure assay showed up-regulation of Id-1 leading to improved migration abilities of bladder cancer cells under chemotherapy. Our results suggest that up-regulation of Id-1 in bladder cancer cells lead to increased cell viability in response to epirubicin by its improved anti-apoptotic role, and down-regulation of Id-1 increases cellular sensitivity to epirubicin by increased anticancer drug-induced apoptosis.en_US
dc.languageengen_US
dc.publisherDemetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/OR/or.htmen_US
dc.relation.ispartofOncology Reportsen_US
dc.subjectApoptosisen_US
dc.subjectBladder Cancer Cellsen_US
dc.subjectChemosensitivityen_US
dc.subjectEpirubicinen_US
dc.subjectId-1en_US
dc.titleThe role of Id-1 in chemosensitivity and epirubicin-induced apoptosis in bladder cancer cellsen_US
dc.typeArticleen_US
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_US
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_US
dc.identifier.authorityWong, YC=rp00316en_US
dc.identifier.authorityLing, MT=rp00449en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.3892/or_00000323en_US
dc.identifier.scopuseid_2-s2.0-67449088929en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67449088929&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume21en_US
dc.identifier.issue4en_US
dc.identifier.spage1053en_US
dc.identifier.epage1059en_US
dc.identifier.isiWOS:000264696000032-
dc.publisher.placeGreeceen_US
dc.identifier.scopusauthoridHu, H=36812244900en_US
dc.identifier.scopusauthoridHan, HY=24477301600en_US
dc.identifier.scopusauthoridWang, YL=9239070700en_US
dc.identifier.scopusauthoridZhang, XP=23394266700en_US
dc.identifier.scopusauthoridChua, CW=9437494600en_US
dc.identifier.scopusauthoridWong, YC=7403041798en_US
dc.identifier.scopusauthoridWang, XF=7501854020en_US
dc.identifier.scopusauthoridLing, MT=7102229780en_US
dc.identifier.scopusauthoridXu, KX=7403282051en_US

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