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

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Title	The role of Id-1 in chemosensitivity and epirubicin-induced apoptosis in bladder cancer cells
Authors	Hu, H1 2 Han, HY1 Wang, YL2 Zhang, XP2 Chua, CW1 Wong, YC1 Wang, XF2 Ling, MT1 Xu, KX2
Keywords	Apoptosis Bladder Cancer Cells Chemosensitivity Epirubicin Id-1
Issue Date	2009
Publisher	Demetrios 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?] DOI: http://dx.doi.org/10.3892/or_00000323
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.
ISSN	1021-335X 2011 Impact Factor: 1.835 2011 SCImago Journal Rankings: 0.196
DOI	http://dx.doi.org/10.3892/or_00000323
ISI Accession Number ID	WOS:000264696000032
References	References in Scopus

DC Field	Value
dc.contributor.author	Hu, H
dc.contributor.author	Han, HY
dc.contributor.author	Wang, YL
dc.contributor.author	Zhang, XP
dc.contributor.author	Chua, CW
dc.contributor.author	Wong, YC
dc.contributor.author	Wang, XF
dc.contributor.author	Ling, MT
dc.contributor.author	Xu, KX
dc.date.accessioned	2012-06-26T05:57:34Z
dc.date.available	2012-06-26T05:57:34Z
dc.date.issued	2009
dc.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.
dc.description.nature	Link_to_subscribed_fulltext
dc.identifier.citation	Oncology Reports, 2009, v. 21 n. 4, p. 1053-1059 [How to Cite?] DOI: http://dx.doi.org/10.3892/or_00000323
dc.identifier.doi	http://dx.doi.org/10.3892/or_00000323
dc.identifier.epage	1059
dc.identifier.isi	WOS:000264696000032
dc.identifier.issn	1021-335X 2011 Impact Factor: 1.835 2011 SCImago Journal Rankings: 0.196
dc.identifier.issue	4
dc.identifier.scopus	eid_2-s2.0-67449088929
dc.identifier.spage	1053
dc.identifier.uri	http://hdl.handle.net/10722/149717
dc.identifier.volume	21
dc.language	eng
dc.publisher	Demetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/OR/or.htm
dc.publisher.place	Greece
dc.relation.ispartof	Oncology Reports
dc.relation.references	References in Scopus
dc.subject	Apoptosis
dc.subject	Bladder Cancer Cells
dc.subject	Chemosensitivity
dc.subject	Epirubicin
dc.subject	Id-1
dc.title	The role of Id-1 in chemosensitivity and epirubicin-induced apoptosis in bladder cancer cells
dc.type	Article

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Author Affiliations

The University of Hong Kong
Peking University

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

The HKU Scholars Hub has contact details for these author(s).