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Article: The role of Id-1 in chemosensitivity and epirubicin-induced apoptosis in bladder cancer cells
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TitleThe role of Id-1 in chemosensitivity and epirubicin-induced apoptosis in bladder cancer cells
 
AuthorsHu, H2 1
Han, HY1
Wang, YL2
Zhang, XP2
Chua, CW1
Wong, YC1
Wang, XF2
Ling, MT1
Xu, KX2
 
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
 
CitationOncology Reports, 2009, v. 21 n. 4, p. 1053-1059 [How to Cite?]
DOI: http://dx.doi.org/10.3892/or_00000323
 
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.
 
ISSN1021-335X
2013 Impact Factor: 2.191
2013 SCImago Journal Rankings: 0.935
 
DOIhttp://dx.doi.org/10.3892/or_00000323
 
ISI Accession Number IDWOS:000264696000032
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorHu, H
 
dc.contributor.authorHan, HY
 
dc.contributor.authorWang, YL
 
dc.contributor.authorZhang, XP
 
dc.contributor.authorChua, CW
 
dc.contributor.authorWong, YC
 
dc.contributor.authorWang, XF
 
dc.contributor.authorLing, MT
 
dc.contributor.authorXu, KX
 
dc.date.accessioned2012-06-26T05:57:34Z
 
dc.date.available2012-06-26T05:57:34Z
 
dc.date.issued2009
 
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.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationOncology Reports, 2009, v. 21 n. 4, p. 1053-1059 [How to Cite?]
DOI: http://dx.doi.org/10.3892/or_00000323
 
dc.identifier.doihttp://dx.doi.org/10.3892/or_00000323
 
dc.identifier.epage1059
 
dc.identifier.isiWOS:000264696000032
 
dc.identifier.issn1021-335X
2013 Impact Factor: 2.191
2013 SCImago Journal Rankings: 0.935
 
dc.identifier.issue4
 
dc.identifier.scopuseid_2-s2.0-67449088929
 
dc.identifier.spage1053
 
dc.identifier.urihttp://hdl.handle.net/10722/149717
 
dc.identifier.volume21
 
dc.languageeng
 
dc.publisherDemetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/OR/or.htm
 
dc.publisher.placeGreece
 
dc.relation.ispartofOncology Reports
 
dc.relation.referencesReferences in Scopus
 
dc.subjectApoptosis
 
dc.subjectBladder Cancer Cells
 
dc.subjectChemosensitivity
 
dc.subjectEpirubicin
 
dc.subjectId-1
 
dc.titleThe role of Id-1 in chemosensitivity and epirubicin-induced apoptosis in bladder cancer cells
 
dc.typeArticle
 
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<contributor.author>Zhang, XP</contributor.author>
<contributor.author>Chua, CW</contributor.author>
<contributor.author>Wong, YC</contributor.author>
<contributor.author>Wang, XF</contributor.author>
<contributor.author>Ling, MT</contributor.author>
<contributor.author>Xu, KX</contributor.author>
<date.accessioned>2012-06-26T05:57:34Z</date.accessioned>
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<description.abstract>Recurrence 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.</description.abstract>
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<subject>Apoptosis</subject>
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Author Affiliations
  1. The University of Hong Kong
  2. Peking University