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Article: Inhibition of tissue factor by siRNA enhances doxorubicin-induced apoptosis in human neuroblastoma

TitleInhibition of tissue factor by siRNA enhances doxorubicin-induced apoptosis in human neuroblastoma
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date2007
Citation
Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi, 2007, v. 28 n. 9, p. 594-597 How to Cite?
AbstractOBJECTIVE: To investigate the regulation of tissue factor (TF) on doxorubicin-induced apoptosis in human neuroblastoma. METHOD: The expression of TF was examined by Western blotting. TF siRNA-pSUPER plasmid was constructed by inserting a specific 19-nt silencing sequence targeting TF gene into pSUPER vector. Transfection of TF siRNA-pSUPER was performed using lipofectamine 2000. The activation of caspase-3 and PARP induced by doxorubicin was tested by Western blotting. The apoptotic cells were stained by Hochest 33342 and counted under fluorescence inverted microscope. RESULTS: (1) Human neuroblastoma cell line SK-N-MC expressed high level of TF. (2) Downregulation of TF expression was achieved by transfection of TF siRNA-pSUPER into SK-N-MC cells in a dose-dependent manner. (3) Cleavage of caspase-3 and PARP was increased in transfected SK-N-MC cell with down-regulation of TF. (4) TF siRNA treatment at 1 microg/ml for 8 h significantly increased apoptotic cell number in transfected SK-N-MC cells compared to that in non-transfected cells (P < 0.05) while exposing to 1 microg/ml doxorubicin for 8 h. CONCLUSIONS: Downregulation of TF expression by specific siRNA vector could increase the cytotoxicity of doxorubicin and enhance doxorubicin-induced apoptosis in human neuroblastoma cells.
Persistent Identifierhttp://hdl.handle.net/10722/92278
ISSN
2015 SCImago Journal Rankings: 0.137

 

DC FieldValueLanguage
dc.contributor.authorFang, Jen_HK
dc.contributor.authorTang, Hen_HK
dc.contributor.authorXia, LHen_HK
dc.contributor.authorZhou, MXen_HK
dc.contributor.authorChen, Yen_HK
dc.contributor.authorWei, WNen_HK
dc.contributor.authorHu, Yen_HK
dc.contributor.authorSong, SJen_HK
dc.date.accessioned2010-09-17T10:41:19Z-
dc.date.available2010-09-17T10:41:19Z-
dc.date.issued2007en_HK
dc.identifier.citationZhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi, 2007, v. 28 n. 9, p. 594-597en_HK
dc.identifier.issn0253-2727en_HK
dc.identifier.urihttp://hdl.handle.net/10722/92278-
dc.description.abstractOBJECTIVE: To investigate the regulation of tissue factor (TF) on doxorubicin-induced apoptosis in human neuroblastoma. METHOD: The expression of TF was examined by Western blotting. TF siRNA-pSUPER plasmid was constructed by inserting a specific 19-nt silencing sequence targeting TF gene into pSUPER vector. Transfection of TF siRNA-pSUPER was performed using lipofectamine 2000. The activation of caspase-3 and PARP induced by doxorubicin was tested by Western blotting. The apoptotic cells were stained by Hochest 33342 and counted under fluorescence inverted microscope. RESULTS: (1) Human neuroblastoma cell line SK-N-MC expressed high level of TF. (2) Downregulation of TF expression was achieved by transfection of TF siRNA-pSUPER into SK-N-MC cells in a dose-dependent manner. (3) Cleavage of caspase-3 and PARP was increased in transfected SK-N-MC cell with down-regulation of TF. (4) TF siRNA treatment at 1 microg/ml for 8 h significantly increased apoptotic cell number in transfected SK-N-MC cells compared to that in non-transfected cells (P < 0.05) while exposing to 1 microg/ml doxorubicin for 8 h. CONCLUSIONS: Downregulation of TF expression by specific siRNA vector could increase the cytotoxicity of doxorubicin and enhance doxorubicin-induced apoptosis in human neuroblastoma cells.en_HK
dc.languageengen_HK
dc.relation.ispartofZhonghua xue ye xue za zhi = Zhonghua xueyexue zazhien_HK
dc.subjectChemicals And Cas Registry Numbersen_HK
dc.titleInhibition of tissue factor by siRNA enhances doxorubicin-induced apoptosis in human neuroblastomaen_HK
dc.typeArticleen_HK
dc.identifier.emailChen, Y:ychenc@hkucc.hku.hken_HK
dc.identifier.authorityChen, Y=rp1318en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid18246814-
dc.identifier.scopuseid_2-s2.0-70449847746en_HK
dc.identifier.volume28en_HK
dc.identifier.issue9en_HK
dc.identifier.spage594en_HK
dc.identifier.epage597en_HK

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