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Article: Effect of p16INK4a on chemosensitivity in nasopharyngeal carcinoma cells.

TitleEffect of p16INK4a on chemosensitivity in nasopharyngeal carcinoma cells.
Authors
Issue Date2000
PublisherSpandidos Publications. The Journal's web site is located at http://www.spandidos-publications.com/ijo/
Citation
International Journal Of Oncology, 2000, v. 17 n. 1, p. 135-140 How to Cite?
AbstractThe p16INK4a tumor suppressor gene is frequently inactivated in nasopharyngeal carcinoma (NPC) and hence it may play an important role in the suppression of this tumor. In order to study the effect of p16INK4a restoration in NPC cells, full-length human p16INK4a gene was transfected into a NPC cell line, CNE1. Four individual clones with differential levels of p16INK4a protein expression, were selected for further studies. The introduction of p16INK4a into CNE1 cells induced growth suppression through G0/G1 cell cycle arrest; however, the cell growth rate was not correlated to the levels of p16INK4a protein expression. To study whether transfection of p16INK4a could protect NPC cells from radiation, cisplatin and 5-fluorouracil (5FU), the cellular sensitivity of p16INK4a transfectants and vector control were investigated. An increase in sensitivity to 5FU was observed (2-fold compared to IC50) in all 4 clones compared to vector-transfected control. P16INK4a transfection also resulted in increased sensitivity to cisplatin (1.5-1.8-fold) in 3 out of 4 cell lines. However, no difference in radiosensitivity was found between the p16INK4a transfectants and the control. These findings indicate that p16INK4a suppresses NPC cell growth through G0/G1 arrest and modulating cellular response to chemotherapeutic drugs in NPC cells. Therefore, restoration of p16INK4a may have a therapeutic purpose in the treatment of NPC.
Persistent Identifierhttp://hdl.handle.net/10722/148207
ISSN
2015 Impact Factor: 3.018
2015 SCImago Journal Rankings: 1.270
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChow, LSen_HK
dc.contributor.authorWang, Xen_HK
dc.contributor.authorKwong, DLen_HK
dc.contributor.authorSham, JSen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorNicholls, JMen_HK
dc.date.accessioned2012-05-29T06:11:30Z-
dc.date.available2012-05-29T06:11:30Z-
dc.date.issued2000en_HK
dc.identifier.citationInternational Journal Of Oncology, 2000, v. 17 n. 1, p. 135-140en_HK
dc.identifier.issn1019-6439en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148207-
dc.description.abstractThe p16INK4a tumor suppressor gene is frequently inactivated in nasopharyngeal carcinoma (NPC) and hence it may play an important role in the suppression of this tumor. In order to study the effect of p16INK4a restoration in NPC cells, full-length human p16INK4a gene was transfected into a NPC cell line, CNE1. Four individual clones with differential levels of p16INK4a protein expression, were selected for further studies. The introduction of p16INK4a into CNE1 cells induced growth suppression through G0/G1 cell cycle arrest; however, the cell growth rate was not correlated to the levels of p16INK4a protein expression. To study whether transfection of p16INK4a could protect NPC cells from radiation, cisplatin and 5-fluorouracil (5FU), the cellular sensitivity of p16INK4a transfectants and vector control were investigated. An increase in sensitivity to 5FU was observed (2-fold compared to IC50) in all 4 clones compared to vector-transfected control. P16INK4a transfection also resulted in increased sensitivity to cisplatin (1.5-1.8-fold) in 3 out of 4 cell lines. However, no difference in radiosensitivity was found between the p16INK4a transfectants and the control. These findings indicate that p16INK4a suppresses NPC cell growth through G0/G1 arrest and modulating cellular response to chemotherapeutic drugs in NPC cells. Therefore, restoration of p16INK4a may have a therapeutic purpose in the treatment of NPC.en_HK
dc.languageengen_US
dc.publisherSpandidos Publications. The Journal's web site is located at http://www.spandidos-publications.com/ijo/en_HK
dc.relation.ispartofInternational journal of oncologyen_HK
dc.subject.meshCarrier Proteins - Genetics - Physiologyen_US
dc.subject.meshCell Cycle - Drug Effects - Physiologyen_US
dc.subject.meshCell Division - Drug Effects - Physiologyen_US
dc.subject.meshCell Survival - Drug Effects - Physiologyen_US
dc.subject.meshCisplatin - Toxicityen_US
dc.subject.meshClone Cellsen_US
dc.subject.meshCyclin-Dependent Kinase Inhibitor P16en_US
dc.subject.meshCyclin-Dependent Kinases - Antagonists & Inhibitorsen_US
dc.subject.meshFluorouracil - Toxicityen_US
dc.subject.meshGenes, Tumor Suppressoren_US
dc.subject.meshHumansen_US
dc.subject.meshNasopharyngeal Neoplasmsen_US
dc.subject.meshRecombinant Proteins - Metabolismen_US
dc.subject.meshTransfectionen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.titleEffect of p16INK4a on chemosensitivity in nasopharyngeal carcinoma cells.en_HK
dc.typeArticleen_HK
dc.identifier.emailKwong, DL:dlwkwong@hku.hken_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.emailNicholls, JM:nicholls@pathology.hku.hken_HK
dc.identifier.authorityKwong, DL=rp00414en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityNicholls, JM=rp00364en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid10853030-
dc.identifier.scopuseid_2-s2.0-0034223549en_HK
dc.identifier.hkuros52810-
dc.identifier.volume17en_HK
dc.identifier.issue1en_HK
dc.identifier.spage135en_HK
dc.identifier.epage140en_HK
dc.identifier.isiWOS:000087552300020-
dc.publisher.placeGreeceen_HK
dc.identifier.scopusauthoridChow, LS=7202533094en_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK
dc.identifier.scopusauthoridKwong, DL=15744231600en_HK
dc.identifier.scopusauthoridSham, JS=24472255400en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridNicholls, JM=7201463077en_HK

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