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Conference Paper: Suppression of tumorigenesis and metastasis of hepatocellular carcinoma by shRNA interference targeting on inhibition of homeoprotein Six1

TitleSuppression of tumorigenesis and metastasis of hepatocellular carcinoma by shRNA interference targeting on inhibition of homeoprotein Six1
Authors
Issue Date2007
PublisherAmerican Association for Cancer Research.
Citation
The 98th Annual Meeting of the American Association for Cancer Research (AACR 2007), Los Angeles, CA., 14-18 April 2007. In Cancer Research, 2007, v. 67 n. 9S, abstract no. 2184 How to Cite?
AbstractWe previously demonstrated that overexpression of homeoprotein Six1 in hepatocellular carcinoma (HCC) patients is associated with venous infiltration, later pathologic tumor metastasis (pTNM) stage and poor overall survival rate (Ng et al., 2006). In this study, short hairpin RNA (shRNA) interference approach was used to suppress the expression of Six1 in a HCC cell line MHCC97L which is capable of local and distant metastases. Stable transfectant MHCC97L-shSix1carrying Six1 specific shRNA plasmid exhibited suppression of Six1 expression to about 40% of the control cell line MHCC97L. In vitro functional assays demonstrated that the growth rate and proliferation ability of MHCC97L-shSix1 were markedly suppressed comparing with the control cells. Furthermore, noticeable decrease in cell motility and invasiveness were observed in MHCC97L-shSix1. Data from in vivo xenograft tumorigenesis model demonstrated that the growth rate of subcutaneous xenograft in MHCC97L-shSix1 group was significantly reduced (P<0.01). Spontaneous metastasis models indicated that targeting Six1 suppression significantly reduced the tumor volume (P < 0.01) and the pulmonary metastasis in MHCC97L-shSix1 group (P=0.026). Our data suggested that Six1 might function involved in tumorigenesis and metastasis of HCC. Suppression of Six1 leading to the reduction of in vitro and in vivo metastatic ability of MHCC97L implied its potential therapeutic application on treatment of HCC metastasis.
Persistent Identifierhttp://hdl.handle.net/10722/107705
ISSN
2023 Impact Factor: 12.5
2023 SCImago Journal Rankings: 3.468

 

DC FieldValueLanguage
dc.contributor.authorNg, TPen_HK
dc.contributor.authorMan, Ken_HK
dc.contributor.authorCheng, Qen_HK
dc.contributor.authorSun, Ben_HK
dc.contributor.authorLee, KWen_HK
dc.contributor.authorPoon, RTPen_HK
dc.contributor.authorLo, CMen_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2010-09-26T00:08:57Z-
dc.date.available2010-09-26T00:08:57Z-
dc.date.issued2007en_HK
dc.identifier.citationThe 98th Annual Meeting of the American Association for Cancer Research (AACR 2007), Los Angeles, CA., 14-18 April 2007. In Cancer Research, 2007, v. 67 n. 9S, abstract no. 2184-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/107705-
dc.description.abstractWe previously demonstrated that overexpression of homeoprotein Six1 in hepatocellular carcinoma (HCC) patients is associated with venous infiltration, later pathologic tumor metastasis (pTNM) stage and poor overall survival rate (Ng et al., 2006). In this study, short hairpin RNA (shRNA) interference approach was used to suppress the expression of Six1 in a HCC cell line MHCC97L which is capable of local and distant metastases. Stable transfectant MHCC97L-shSix1carrying Six1 specific shRNA plasmid exhibited suppression of Six1 expression to about 40% of the control cell line MHCC97L. In vitro functional assays demonstrated that the growth rate and proliferation ability of MHCC97L-shSix1 were markedly suppressed comparing with the control cells. Furthermore, noticeable decrease in cell motility and invasiveness were observed in MHCC97L-shSix1. Data from in vivo xenograft tumorigenesis model demonstrated that the growth rate of subcutaneous xenograft in MHCC97L-shSix1 group was significantly reduced (P<0.01). Spontaneous metastasis models indicated that targeting Six1 suppression significantly reduced the tumor volume (P < 0.01) and the pulmonary metastasis in MHCC97L-shSix1 group (P=0.026). Our data suggested that Six1 might function involved in tumorigenesis and metastasis of HCC. Suppression of Six1 leading to the reduction of in vitro and in vivo metastatic ability of MHCC97L implied its potential therapeutic application on treatment of HCC metastasis.-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research.-
dc.relation.ispartofCancer Researchen_HK
dc.titleSuppression of tumorigenesis and metastasis of hepatocellular carcinoma by shRNA interference targeting on inhibition of homeoprotein Six1en_HK
dc.typeConference_Paperen_HK
dc.identifier.emailNg, TP: ledodes@hku.hken_HK
dc.identifier.emailMan, K: kwanman@hkucc.hku.hken_HK
dc.identifier.emailCheng, Q: qiaocheng@hotmail.comen_HK
dc.identifier.emailSun, B: sbs5cycl@hotmail.comen_HK
dc.identifier.emailLee, KW: tkwlee@hkucc.hku.hken_HK
dc.identifier.emailPoon, RTP: poontp@hkucc.hku.hken_HK
dc.identifier.emailLo, CM: chungmlo@hkucc.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityMan, K=rp00417en_HK
dc.identifier.authorityLee, KW=rp00447en_HK
dc.identifier.authorityPoon, RTP=rp00446en_HK
dc.identifier.authorityLo, CM=rp00412en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.identifier.hkuros135900en_HK
dc.identifier.volume67-
dc.identifier.issue9 suppl.-
dc.identifier.issnl0008-5472-

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