File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
  • Find via Find It@HKUL
Supplementary

Conference Paper: GnRH enhances matrix metalloproteinases-dependent invasion of human ovarian cancer cells

TitleGnRH enhances matrix metalloproteinases-dependent invasion of human ovarian cancer cells
Authors
Issue Date2006
PublisherHong Kong Medical Association. The Journal's web site is located at http://www.hkmj.org/
Citation
The 4th International Huaxia Congress of Endocrinology, Hong Kong, China, 15-18 December 2006, In Hong Kong Medical Journal, v.12 suppl. 4, p. 169, abstract no. P211 How to Cite?
AbstractObjectives: To investigate the contribution of GnRH in the invasive behavior of human ovarian cancer cells and to unveil the mechanism underlying this process. Methods: In vitro migration and cell invasion assays were performed with two human ovarian cancer cell lines CaOV-3 and OVCAR-3 in the presence of GnRH agonist. RT-PCR, Western blot, and gelatin zymography were used to investigate the effect of GnRH on metastasis-related proteinases, matrix metalloproteinase (MMP)-2 and MMP-9. The signaling pathway involved was identified by using specific small molecule inhibitors and dominant negative mutants. Results: The in vitro assays revealed a biphasic nature of GnRH; low concentrations of GnRH agonist increased cell motility and invasiveness of CaOV-3 and OVCAR-3, but the stimulatory effect was insignificant at higher concentrations. Moreover, we demonstrated that expression and activation of MMP-2 and MMP-9 were functionally related to GnRH-mediated invasion, and this was through the c-Jun N-terminal kinase signaling pathway. Conclusion: These results suggest a novel role of GnRH signaling cascade in the invasive phenotype and motility of human ovarian cancer cells.
Persistent Identifierhttp://hdl.handle.net/10722/110591
ISSN
2015 Impact Factor: 0.887
2015 SCImago Journal Rankings: 0.279

 

DC FieldValueLanguage
dc.contributor.authorCheung, WTen_HK
dc.contributor.authorLeung, PCKen_HK
dc.contributor.authorWong, ASTen_HK
dc.date.accessioned2010-09-26T02:12:29Z-
dc.date.available2010-09-26T02:12:29Z-
dc.date.issued2006en_HK
dc.identifier.citationThe 4th International Huaxia Congress of Endocrinology, Hong Kong, China, 15-18 December 2006, In Hong Kong Medical Journal, v.12 suppl. 4, p. 169, abstract no. P211-
dc.identifier.issn1024-2708-
dc.identifier.urihttp://hdl.handle.net/10722/110591-
dc.description.abstractObjectives: To investigate the contribution of GnRH in the invasive behavior of human ovarian cancer cells and to unveil the mechanism underlying this process. Methods: In vitro migration and cell invasion assays were performed with two human ovarian cancer cell lines CaOV-3 and OVCAR-3 in the presence of GnRH agonist. RT-PCR, Western blot, and gelatin zymography were used to investigate the effect of GnRH on metastasis-related proteinases, matrix metalloproteinase (MMP)-2 and MMP-9. The signaling pathway involved was identified by using specific small molecule inhibitors and dominant negative mutants. Results: The in vitro assays revealed a biphasic nature of GnRH; low concentrations of GnRH agonist increased cell motility and invasiveness of CaOV-3 and OVCAR-3, but the stimulatory effect was insignificant at higher concentrations. Moreover, we demonstrated that expression and activation of MMP-2 and MMP-9 were functionally related to GnRH-mediated invasion, and this was through the c-Jun N-terminal kinase signaling pathway. Conclusion: These results suggest a novel role of GnRH signaling cascade in the invasive phenotype and motility of human ovarian cancer cells.-
dc.languageengen_HK
dc.publisherHong Kong Medical Association. The Journal's web site is located at http://www.hkmj.org/-
dc.relation.ispartofHong Kong Medical Journalen_HK
dc.titleGnRH enhances matrix metalloproteinases-dependent invasion of human ovarian cancer cellsen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailWong, AST: awong1@hkucc.hku.hken_HK
dc.identifier.authorityWong, AST=rp00805en_HK
dc.identifier.hkuros130203en_HK
dc.identifier.volume12-
dc.identifier.issuesuppl. 4-
dc.identifier.spage169, abstract no. P211-
dc.identifier.epage169, abstract no. P211-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats