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Article: FTY720: A promising agent for treatment of metastatic hepatocellular carcinoma

TitleFTY720: A promising agent for treatment of metastatic hepatocellular carcinoma
Authors
Issue Date2005
PublisherAmerican Association for Cancer Research.
Citation
Clinical Cancer Research, 2005, v. 11 n. 23, p. 8458-8466 How to Cite?
AbstractPurpose: Recurrence after resection and metastasis are common in hepatocellular carcinoma and are associated with poor prognosis. Therefore, effective treatment is urgently needed for improvement of patients' survival. Previously, we reported that FTY720 has an antimetastatic effect on hepatocellular carcinoma cell line through down-regulation of Rac signaling pathway. This study aims to investigate the in vivo antimetastatic potential of FTY720 in an orthotopic nude mice model using metastatic human hepatocellular carcinoma cell lines MHCC-97L (lower metastatic potential) and MHCC-97H (higher metastatic potential). Experimental Design: The nude mice bearing liver tumors were randomized into a treatment group and a control group, each with 12 mice. FTY720 was administered at a dosage of 5 or 10 mg/kg via i.p. injection after 7 days of tumor inoculation. Thirty-five days later, the mice were sacrificed for record of intrahepatic and pulmonary metastases. Results: After 35 days of FTY720 treatment at the dosages of 5 and 10 mg/kg, all 12 mice in the treatment group were alive and well. FTY720 at the dosages of 5 and 10 mg/kg significantly suppressed the tumor volume and intrahepatic and pulmonary metastases in the metastatic nude mice model. FTY720 suppressed intrahepatic and pulmonary metastases by inhibition of Rac expression, which at least in part down-regulated the vascular endothelial growth factor expression and CD34 staining in a dose-dependent manner. Conclusion: FTY720 is a promising novel therapeutic drug for treatment of hepatocellular carcinoma metastasis. © 2005 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/88434
ISSN
2014 Impact Factor: 8.722
2013 SCImago Journal Rankings: 5.150
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLee, TKen_HK
dc.contributor.authorMan, Ken_HK
dc.contributor.authorHo, JWen_HK
dc.contributor.authorWang, XHen_HK
dc.contributor.authorPoon, RTPen_HK
dc.contributor.authorXu, Yen_HK
dc.contributor.authorNg, KTen_HK
dc.contributor.authorChu, ACen_HK
dc.contributor.authorSun, CKen_HK
dc.contributor.authorNg, IOen_HK
dc.contributor.authorSun, HCen_HK
dc.contributor.authorTang, ZYen_HK
dc.contributor.authorXu, Ren_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2010-09-06T09:43:19Z-
dc.date.available2010-09-06T09:43:19Z-
dc.date.issued2005en_HK
dc.identifier.citationClinical Cancer Research, 2005, v. 11 n. 23, p. 8458-8466en_HK
dc.identifier.issn1078-0432en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88434-
dc.description.abstractPurpose: Recurrence after resection and metastasis are common in hepatocellular carcinoma and are associated with poor prognosis. Therefore, effective treatment is urgently needed for improvement of patients' survival. Previously, we reported that FTY720 has an antimetastatic effect on hepatocellular carcinoma cell line through down-regulation of Rac signaling pathway. This study aims to investigate the in vivo antimetastatic potential of FTY720 in an orthotopic nude mice model using metastatic human hepatocellular carcinoma cell lines MHCC-97L (lower metastatic potential) and MHCC-97H (higher metastatic potential). Experimental Design: The nude mice bearing liver tumors were randomized into a treatment group and a control group, each with 12 mice. FTY720 was administered at a dosage of 5 or 10 mg/kg via i.p. injection after 7 days of tumor inoculation. Thirty-five days later, the mice were sacrificed for record of intrahepatic and pulmonary metastases. Results: After 35 days of FTY720 treatment at the dosages of 5 and 10 mg/kg, all 12 mice in the treatment group were alive and well. FTY720 at the dosages of 5 and 10 mg/kg significantly suppressed the tumor volume and intrahepatic and pulmonary metastases in the metastatic nude mice model. FTY720 suppressed intrahepatic and pulmonary metastases by inhibition of Rac expression, which at least in part down-regulated the vascular endothelial growth factor expression and CD34 staining in a dose-dependent manner. Conclusion: FTY720 is a promising novel therapeutic drug for treatment of hepatocellular carcinoma metastasis. © 2005 American Association for Cancer Research.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research.en_HK
dc.relation.ispartofClinical Cancer Researchen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAntigens, CD34 - metabolismen_HK
dc.subject.meshCarcinoma, Hepatocellular - drug therapy - metabolism - secondaryen_HK
dc.subject.meshDisease Models, Animalen_HK
dc.subject.meshDown-Regulationen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunosuppressive Agents - therapeutic useen_HK
dc.subject.meshLiver Neoplasms, Experimental - drug therapy - metabolism - pathologyen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Nudeen_HK
dc.subject.meshMicrocirculationen_HK
dc.subject.meshNeovascularization, Pathologic - prevention & controlen_HK
dc.subject.meshPropylene Glycols - therapeutic useen_HK
dc.subject.meshSphingosine - analogs & derivativesen_HK
dc.subject.meshTumor Cells, Cultureden_HK
dc.subject.meshVascular Endothelial Growth Factor A - metabolismen_HK
dc.subject.meshWound Healingen_HK
dc.subject.meshrac GTP-Binding Proteins - chemistry - metabolismen_HK
dc.titleFTY720: A promising agent for treatment of metastatic hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1078-0432&volume=11&issue=23&spage=8458&epage=8466&date=2005&atitle=FTY720:+a+promising+agent+for+treatment+of+metastatic+hepatocellular+carcinomaen_HK
dc.identifier.emailLee, TK: tkwlee@hkucc.hku.hken_HK
dc.identifier.emailMan, K: kwanman@hku.hken_HK
dc.identifier.emailPoon, RTP: poontp@hku.hken_HK
dc.identifier.emailNg, KT: ledodes@hku.hken_HK
dc.identifier.emailNg, IO: iolng@hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityLee, TK=rp00447en_HK
dc.identifier.authorityMan, K=rp00417en_HK
dc.identifier.authorityPoon, RTP=rp00446en_HK
dc.identifier.authorityNg, KT=rp01720en_HK
dc.identifier.authorityNg, IO=rp00335en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1158/1078-0432.CCR-05-0447en_HK
dc.identifier.pmid16322309en_HK
dc.identifier.scopuseid_2-s2.0-28544451354en_HK
dc.identifier.hkuros116899en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-28544451354&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume11en_HK
dc.identifier.issue23en_HK
dc.identifier.spage8458en_HK
dc.identifier.epage8466en_HK
dc.identifier.isiWOS:000233701300033-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLee, TK=7501439435en_HK
dc.identifier.scopusauthoridMan, K=7101754072en_HK
dc.identifier.scopusauthoridHo, JW=7402649982en_HK
dc.identifier.scopusauthoridWang, XH=7501854829en_HK
dc.identifier.scopusauthoridPoon, RTP=7103097223en_HK
dc.identifier.scopusauthoridXu, Y=7407810176en_HK
dc.identifier.scopusauthoridNg, KT=7403178513en_HK
dc.identifier.scopusauthoridChu, AC=9740303300en_HK
dc.identifier.scopusauthoridSun, CK=7404248685en_HK
dc.identifier.scopusauthoridNg, IO=7102753722en_HK
dc.identifier.scopusauthoridSun, HC=7404827176en_HK
dc.identifier.scopusauthoridTang, ZY=15752346400en_HK
dc.identifier.scopusauthoridXu, R=8652263200en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK

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