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- PMID: 12678717
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Article: Induction of senescent-like growth arrest as a new target in anticancer treatment
Title | Induction of senescent-like growth arrest as a new target in anticancer treatment |
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Authors | |
Issue Date | 2003 |
Publisher | Bentham 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? |
Abstract | Replicative 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 Identifier | http://hdl.handle.net/10722/67575 |
ISSN | 2023 Impact Factor: 2.3 2023 SCImago Journal Rankings: 0.650 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | Wang, X | en_HK |
dc.contributor.author | Tsao, SW | en_HK |
dc.contributor.author | Wong, YC | en_HK |
dc.contributor.author | Cheung, ALM | en_HK |
dc.date.accessioned | 2010-09-06T05:56:21Z | - |
dc.date.available | 2010-09-06T05:56:21Z | - |
dc.date.issued | 2003 | en_HK |
dc.identifier.citation | Current Cancer Drug Targets, 2003, v. 3 n. 2, p. 153-159 | en_HK |
dc.identifier.issn | 1568-0096 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/67575 | - |
dc.description.abstract | Replicative 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.language | eng | en_HK |
dc.publisher | Bentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/ccdt/index.htm | en_HK |
dc.relation.ispartof | Current Cancer Drug Targets | en_HK |
dc.subject.mesh | Animals | en_HK |
dc.subject.mesh | Antineoplastic Agents - pharmacology | en_HK |
dc.subject.mesh | Apoptosis - drug effects | en_HK |
dc.subject.mesh | Cell Aging - drug effects - physiology | en_HK |
dc.subject.mesh | Cell Division - drug effects | en_HK |
dc.subject.mesh | Humans | en_HK |
dc.title | Induction of senescent-like growth arrest as a new target in anticancer treatment | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://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+treatment | en_HK |
dc.identifier.email | Tsao, SW:gswtsao@hkucc.hku.hk | en_HK |
dc.identifier.email | Wong, YC:ycwong@hkucc.hku.hk | en_HK |
dc.identifier.email | Cheung, ALM:lmcheung@hkucc.hku.hk | en_HK |
dc.identifier.authority | Tsao, SW=rp00399 | en_HK |
dc.identifier.authority | Wong, YC=rp00316 | en_HK |
dc.identifier.authority | Cheung, ALM=rp00332 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.2174/1568009033482001 | en_HK |
dc.identifier.pmid | 12678717 | - |
dc.identifier.scopus | eid_2-s2.0-0037380878 | en_HK |
dc.identifier.hkuros | 88938 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0037380878&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 3 | en_HK |
dc.identifier.issue | 2 | en_HK |
dc.identifier.spage | 153 | en_HK |
dc.identifier.epage | 159 | en_HK |
dc.identifier.isi | WOS:000209052800005 | - |
dc.publisher.place | Netherlands | en_HK |
dc.identifier.scopusauthorid | Wang, X=7501854829 | en_HK |
dc.identifier.scopusauthorid | Tsao, SW=7102813116 | en_HK |
dc.identifier.scopusauthorid | Wong, YC=7403041798 | en_HK |
dc.identifier.scopusauthorid | Cheung, ALM=7401806497 | en_HK |
dc.identifier.issnl | 1568-0096 | - |