File Download
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: Mechanism of differential sensitivity to cisplatin in nasopharyngeal carcinoma cells
  • Basic View
  • Metadata View
  • XML View
TitleMechanism of differential sensitivity to cisplatin in nasopharyngeal carcinoma cells
 
AuthorsWang, X1
Masters, JRW1
Wong, YC1
Lo, AKF1
Tsao, SW1
 
Issue Date2001
 
PublisherInternational Institute of Anticancer Research.
 
CitationAnticancer Research, 2001, v. 21 n. 1 A, p. 403-408 [How to Cite?]
 
AbstractCisplatin is used in the treatment of many tumours, including nasopharyngeal carcinoma (NPC). In this study, we studied two nasopharyngeal cancer cell lines with a four-fold difference in sensitivity to cisplatin. Following exposure to cisplatin, the sensitive SUNE1 cell line underwent apoptosis while the relatively resistant CNE1 line died through mitotic cell death. No differences were seen in telomere length or in the cell cycle distribution after cisplatin treatment. However, there was an increase in Bax levels in the sensitive cell line SUNE1, while in the resistant line CNE1 that did not undergo apoptosis, Bax levels fell. Our results suggest that upregulation of Bax is associated with the sensitivity of these NPC cells to cisplatin.
 
ISSN0250-7005
2012 Impact Factor: 1.713
2012 SCImago Journal Rankings: 0.659
 
ISI Accession Number IDWOS:000167875900058
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorWang, X
 
dc.contributor.authorMasters, JRW
 
dc.contributor.authorWong, YC
 
dc.contributor.authorLo, AKF
 
dc.contributor.authorTsao, SW
 
dc.date.accessioned2010-09-06T05:58:33Z
 
dc.date.available2010-09-06T05:58:33Z
 
dc.date.issued2001
 
dc.description.abstractCisplatin is used in the treatment of many tumours, including nasopharyngeal carcinoma (NPC). In this study, we studied two nasopharyngeal cancer cell lines with a four-fold difference in sensitivity to cisplatin. Following exposure to cisplatin, the sensitive SUNE1 cell line underwent apoptosis while the relatively resistant CNE1 line died through mitotic cell death. No differences were seen in telomere length or in the cell cycle distribution after cisplatin treatment. However, there was an increase in Bax levels in the sensitive cell line SUNE1, while in the resistant line CNE1 that did not undergo apoptosis, Bax levels fell. Our results suggest that upregulation of Bax is associated with the sensitivity of these NPC cells to cisplatin.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationAnticancer Research, 2001, v. 21 n. 1 A, p. 403-408 [How to Cite?]
 
dc.identifier.epage408
 
dc.identifier.hkuros56940
 
dc.identifier.isiWOS:000167875900058
 
dc.identifier.issn0250-7005
2012 Impact Factor: 1.713
2012 SCImago Journal Rankings: 0.659
 
dc.identifier.issue1 A
 
dc.identifier.openurl
 
dc.identifier.pmid11299769
 
dc.identifier.scopuseid_2-s2.0-0035056857
 
dc.identifier.spage403
 
dc.identifier.urihttp://hdl.handle.net/10722/67821
 
dc.identifier.volume21
 
dc.languageeng
 
dc.publisherInternational Institute of Anticancer Research.
 
dc.publisher.placeGreece
 
dc.relation.ispartofAnticancer Research
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAntineoplastic Agents - pharmacology
 
dc.subject.meshApoptosis - drug effects
 
dc.subject.meshCarcinoma - drug therapy - metabolism - pathology
 
dc.subject.meshCell Cycle - drug effects
 
dc.subject.meshCell Nucleus - ultrastructure
 
dc.subject.meshCisplatin - pharmacology
 
dc.subject.meshDrug Resistance, Neoplasm
 
dc.subject.meshHumans
 
dc.subject.meshKinetics
 
dc.subject.meshNasopharyngeal Neoplasms - drug therapy - metabolism - pathology
 
dc.subject.meshProto-Oncogene Proteins - metabolism
 
dc.subject.meshProto-Oncogene Proteins c-bcl-2 - metabolism
 
dc.subject.meshRadiation-Sensitizing Agents - pharmacology
 
dc.subject.meshTelomere - ultrastructure
 
dc.subject.meshTumor Cells, Cultured
 
dc.subject.meshTumor Stem Cell Assay
 
dc.subject.meshUp-Regulation
 
dc.subject.meshbcl-2-Associated X Protein
 
dc.titleMechanism of differential sensitivity to cisplatin in nasopharyngeal carcinoma cells
 
dc.typeArticle
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Wang, X</contributor.author>
<contributor.author>Masters, JRW</contributor.author>
<contributor.author>Wong, YC</contributor.author>
<contributor.author>Lo, AKF</contributor.author>
<contributor.author>Tsao, SW</contributor.author>
<date.accessioned>2010-09-06T05:58:33Z</date.accessioned>
<date.available>2010-09-06T05:58:33Z</date.available>
<date.issued>2001</date.issued>
<identifier.citation>Anticancer Research, 2001, v. 21 n. 1 A, p. 403-408</identifier.citation>
<identifier.issn>0250-7005</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/67821</identifier.uri>
<description.abstract>Cisplatin is used in the treatment of many tumours, including nasopharyngeal carcinoma (NPC). In this study, we studied two nasopharyngeal cancer cell lines with a four-fold difference in sensitivity to cisplatin. Following exposure to cisplatin, the sensitive SUNE1 cell line underwent apoptosis while the relatively resistant CNE1 line died through mitotic cell death. No differences were seen in telomere length or in the cell cycle distribution after cisplatin treatment. However, there was an increase in Bax levels in the sensitive cell line SUNE1, while in the resistant line CNE1 that did not undergo apoptosis, Bax levels fell. Our results suggest that upregulation of Bax is associated with the sensitivity of these NPC cells to cisplatin.</description.abstract>
<language>eng</language>
<publisher>International Institute of Anticancer Research.</publisher>
<relation.ispartof>Anticancer Research</relation.ispartof>
<subject.mesh>Antineoplastic Agents - pharmacology</subject.mesh>
<subject.mesh>Apoptosis - drug effects</subject.mesh>
<subject.mesh>Carcinoma - drug therapy - metabolism - pathology</subject.mesh>
<subject.mesh>Cell Cycle - drug effects</subject.mesh>
<subject.mesh>Cell Nucleus - ultrastructure</subject.mesh>
<subject.mesh>Cisplatin - pharmacology</subject.mesh>
<subject.mesh>Drug Resistance, Neoplasm</subject.mesh>
<subject.mesh>Humans</subject.mesh>
<subject.mesh>Kinetics</subject.mesh>
<subject.mesh>Nasopharyngeal Neoplasms - drug therapy - metabolism - pathology</subject.mesh>
<subject.mesh>Proto-Oncogene Proteins - metabolism</subject.mesh>
<subject.mesh>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject.mesh>
<subject.mesh>Radiation-Sensitizing Agents - pharmacology</subject.mesh>
<subject.mesh>Telomere - ultrastructure</subject.mesh>
<subject.mesh>Tumor Cells, Cultured</subject.mesh>
<subject.mesh>Tumor Stem Cell Assay</subject.mesh>
<subject.mesh>Up-Regulation</subject.mesh>
<subject.mesh>bcl-2-Associated X Protein</subject.mesh>
<title>Mechanism of differential sensitivity to cisplatin in nasopharyngeal carcinoma cells</title>
<type>Article</type>
<identifier.openurl>http://library.hku.hk:4550/resserv?sid=HKU:IR&amp;issn=0250-7005&amp;volume=21&amp;spage=403&amp;epage=408&amp;date=2001&amp;atitle=Mechanism+of+differential+sensitivity+to+cisplatin+in+nasopharyngeal+carcinoma+cells</identifier.openurl>
<description.nature>Link_to_subscribed_fulltext</description.nature>
<identifier.pmid>11299769</identifier.pmid>
<identifier.scopus>eid_2-s2.0-0035056857</identifier.scopus>
<identifier.hkuros>56940</identifier.hkuros>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-0035056857&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>21</identifier.volume>
<identifier.issue>1 A</identifier.issue>
<identifier.spage>403</identifier.spage>
<identifier.epage>408</identifier.epage>
<identifier.isi>WOS:000167875900058</identifier.isi>
<publisher.place>Greece</publisher.place>
</item>
Author Affiliations
  1. The University of Hong Kong