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Article: Induction of senescent-like growth arrest as a new target in anticancer treatment

TitleInduction of senescent-like growth arrest as a new target in anticancer treatment
Authors
Issue Date2003
PublisherBentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/ccdt/index.htm
Citation
Current Cancer Drug Targets, 2003, v. 3 n. 2, p. 153-159 How to Cite?
AbstractReplicative senescence is a programmed cellular response in normal cells, the induction of which depends on the accumulated number of cell divisions. Unlike cells undergoing apoptosis, senescent cells have a large and flat morphology, express acidic β-galactosidase (β-gal) and show a permanent cell cycle G1 phase arrest. Recently, senescent-like growth arrest has been observed in many types of tumor cell lines after exposure to certain chemotherapeutic drugs. These senescent-like cancer cells show similar morphology, growth arrest and β-gal expression to normal cells undergoing replicative senescence. However, unlike replicative senescence during the aging process, the chemodrug-induced senescent-like growth arrest is independent of cell cycle distribution, telomere length or cell cycle inhibitors. These observations suggest that induction of senescentlike response may provide a novel target leading to permanent growth arrest in cancer cells. So far, cell lines derived from more than 14 types of cancers have shown senescent-like growth arrest by either introduction of tumor suppressor genes or treatment with chemotherapeutic drugs. In addition, the drug-induced β-gal expression has been correlated with cancer cells undergoing terminal senescent-like growth arrest, which provides a possible marker for this process. This review will describe the evidence on senescent-like growth arrest in human cancer cells and the molecular changes that differ between chemodrug-induced senescent-like growth arrest and apoptosis. In addition, the possible factors and mechanisms involved in this process are also discussed. Finally, the implications on how senescent-like growth arrest might be exploited as a possible new target for anti-cancer drugs are addressed.
Persistent Identifierhttp://hdl.handle.net/10722/67575
ISSN
2015 Impact Factor: 3.707
2015 SCImago Journal Rankings: 1.537
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, Xen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorWong, YCen_HK
dc.contributor.authorCheung, ALMen_HK
dc.date.accessioned2010-09-06T05:56:21Z-
dc.date.available2010-09-06T05:56:21Z-
dc.date.issued2003en_HK
dc.identifier.citationCurrent Cancer Drug Targets, 2003, v. 3 n. 2, p. 153-159en_HK
dc.identifier.issn1568-0096en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67575-
dc.description.abstractReplicative senescence is a programmed cellular response in normal cells, the induction of which depends on the accumulated number of cell divisions. Unlike cells undergoing apoptosis, senescent cells have a large and flat morphology, express acidic β-galactosidase (β-gal) and show a permanent cell cycle G1 phase arrest. Recently, senescent-like growth arrest has been observed in many types of tumor cell lines after exposure to certain chemotherapeutic drugs. These senescent-like cancer cells show similar morphology, growth arrest and β-gal expression to normal cells undergoing replicative senescence. However, unlike replicative senescence during the aging process, the chemodrug-induced senescent-like growth arrest is independent of cell cycle distribution, telomere length or cell cycle inhibitors. These observations suggest that induction of senescentlike response may provide a novel target leading to permanent growth arrest in cancer cells. So far, cell lines derived from more than 14 types of cancers have shown senescent-like growth arrest by either introduction of tumor suppressor genes or treatment with chemotherapeutic drugs. In addition, the drug-induced β-gal expression has been correlated with cancer cells undergoing terminal senescent-like growth arrest, which provides a possible marker for this process. This review will describe the evidence on senescent-like growth arrest in human cancer cells and the molecular changes that differ between chemodrug-induced senescent-like growth arrest and apoptosis. In addition, the possible factors and mechanisms involved in this process are also discussed. Finally, the implications on how senescent-like growth arrest might be exploited as a possible new target for anti-cancer drugs are addressed.en_HK
dc.languageengen_HK
dc.publisherBentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/ccdt/index.htmen_HK
dc.relation.ispartofCurrent Cancer Drug Targetsen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAntineoplastic Agents - pharmacologyen_HK
dc.subject.meshApoptosis - drug effectsen_HK
dc.subject.meshCell Aging - drug effects - physiologyen_HK
dc.subject.meshCell Division - drug effectsen_HK
dc.subject.meshHumansen_HK
dc.titleInduction of senescent-like growth arrest as a new target in anticancer treatmenten_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1568-0096&volume=3&spage=153&epage=160&date=2003&atitle=Induction+of+senescent-like+growth+arrest+as+a+new+target+in+anticancer+treatmenten_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.emailCheung, ALM:lmcheung@hkucc.hku.hken_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.authorityCheung, ALM=rp00332en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.2174/1568009033482001en_HK
dc.identifier.pmid12678717-
dc.identifier.scopuseid_2-s2.0-0037380878en_HK
dc.identifier.hkuros88938en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037380878&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume3en_HK
dc.identifier.issue2en_HK
dc.identifier.spage153en_HK
dc.identifier.epage159en_HK
dc.identifier.isiWOS:000209052800005-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK
dc.identifier.scopusauthoridCheung, ALM=7401806497en_HK

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