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Conference Paper: Zic2 synergistically enhances Hedgehog signaling pathway through sequestration of Gli1 in the nucleus of cervical cancer cells

TitleZic2 synergistically enhances Hedgehog signaling pathway through sequestration of Gli1 in the nucleus of cervical cancer cells
Authors
Issue Date2009
PublisherAmerican Association for Cancer Research
Citation
The American Association for Cancer Research Annual Meeting, Denver, CO, 18-22 April 2009. In Cancer Research, 2009, v. 69, Abstract no. 5285 How to Cite?
AbstractCervical cancer is a potentially preventable disease but remains the second most common female malignancy. Human papillomavirus (HPV) is the crucial etiological agent in cervical cancer. However, evidence suggests that HPV infection alone is insufficient to induce malignant changes. Therefore, the transformation from low-grade lesion to invasive cancer must involve other cellular genetic lesions alterating signal transduction pathways. We have recently identified a candidate zinc finger oncogene Zic2 remarkably upregulated and was associated with the Hedgehog (Hh) signaling pathway in cervical cancer cells. Intriguingly, co-immunoprecipitation, subcellular fractionation and immunofluorescent analyses revealed that Zic2 could physically interact and sequester Gli1 in the nucleus which in turn increased Gli-mediated transcriptional activities. This was supported by transient reporter assays that Zic2 significantly increased Gli-promoter luciferase activity in a dose-dependent manner. Functionally, enforced expression of Zic2 in cervical cancer cells resulted in substantial enhancement of cell proliferation rate, anchorage-independent growth ability, and upregulation of the Hh pathway downstream targets. Taken together, these results suggest that Zic2 synergistically enhances the Hh signaling activity through retaining Gli1 in the nucleus of cervical cancer cells.
Persistent Identifierhttp://hdl.handle.net/10722/63553
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorChan, DWen_HK
dc.contributor.authorYip, CTen_HK
dc.contributor.authorLiu, VWSen_HK
dc.contributor.authorNgan, HYSen_HK
dc.date.accessioned2010-07-13T04:26:17Z-
dc.date.available2010-07-13T04:26:17Z-
dc.date.issued2009en_HK
dc.identifier.citationThe American Association for Cancer Research Annual Meeting, Denver, CO, 18-22 April 2009. In Cancer Research, 2009, v. 69, Abstract no. 5285-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/63553-
dc.description.abstractCervical cancer is a potentially preventable disease but remains the second most common female malignancy. Human papillomavirus (HPV) is the crucial etiological agent in cervical cancer. However, evidence suggests that HPV infection alone is insufficient to induce malignant changes. Therefore, the transformation from low-grade lesion to invasive cancer must involve other cellular genetic lesions alterating signal transduction pathways. We have recently identified a candidate zinc finger oncogene Zic2 remarkably upregulated and was associated with the Hedgehog (Hh) signaling pathway in cervical cancer cells. Intriguingly, co-immunoprecipitation, subcellular fractionation and immunofluorescent analyses revealed that Zic2 could physically interact and sequester Gli1 in the nucleus which in turn increased Gli-mediated transcriptional activities. This was supported by transient reporter assays that Zic2 significantly increased Gli-promoter luciferase activity in a dose-dependent manner. Functionally, enforced expression of Zic2 in cervical cancer cells resulted in substantial enhancement of cell proliferation rate, anchorage-independent growth ability, and upregulation of the Hh pathway downstream targets. Taken together, these results suggest that Zic2 synergistically enhances the Hh signaling activity through retaining Gli1 in the nucleus of cervical cancer cells.-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research-
dc.relation.ispartofCancer Research-
dc.titleZic2 synergistically enhances Hedgehog signaling pathway through sequestration of Gli1 in the nucleus of cervical cancer cellsen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailChan, DW: dwchan@hkucc.hku.hken_HK
dc.identifier.emailYip, CT: bo_yct@yahoo.com.hken_HK
dc.identifier.emailLiu, VWS: vwsliu@hkusua.hku.hken_HK
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hken_HK
dc.identifier.authorityChan, DW=rp00543en_HK
dc.identifier.authorityLiu, VWS=rp00341en_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.identifier.hkuros158039en_HK

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