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Article: Increased expression of PITX2 transcription factor contributes to ovarian cancer progression
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TitleIncreased expression of PITX2 transcription factor contributes to ovarian cancer progression
 
AuthorsFung, FKC
Chan, DW
Liu, VWS
Leung, THY
Cheung, ANY
Ngan, HYS
 
Issue Date2012
 
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
CitationPLoS One, 2012, v. 7 n. 5, article no. e37076 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0037076
 
AbstractBACKGROUND: Paired-like homeodomain 2 (PITX2) is a bicoid homeodomain transcription factor which plays an essential role in maintaining embryonic left-right asymmetry during vertebrate embryogenesis. However, emerging evidence suggests that the aberrant upregulation of PITX2 may be associated with tumor progression, yet the functional role that PITX2 plays in tumorigenesis remains unknown. PRINCIPAL FINDINGS: Using real-time quantitative RT-PCR (Q-PCR), Western blot and immunohistochemical (IHC) analyses, we demonstrated that PITX2 was frequently overexpressed in ovarian cancer samples and cell lines. Clinicopathological correlation showed that the upregulated PITX2 was significantly associated with high-grade (P = 0.023) and clear cell subtype (P = 0.011) using Q-PCR and high-grade (P<0.001) ovarian cancer by IHC analysis. Functionally, enforced expression of PITX2 could promote ovarian cancer cell proliferation, anchorage-independent growth ability, migration/invasion and tumor growth in xenograft model mice. Moreover, enforced expression of PITX2 elevated the cell cycle regulatory proteins such as Cyclin-D1 and C-myc. Conversely, RNAi mediated knockdown of PITX2 in PITX2-high expressing ovarian cancer cells had the opposite effect. CONCLUSION: Our findings suggest that the increased expression PITX2 is involved in ovarian cancer progression through promoting cell growth and cell migration/invasion. Thus, targeting PITX2 may serve as a potential therapeutic modality in the management of high-grade ovarian tumor.
 
ISSN1932-6203
2012 Impact Factor: 3.73
2012 SCImago Journal Rankings: 1.512
 
DOIhttp://dx.doi.org/10.1371/journal.pone.0037076
 
PubMed Central IDPMC3352869
 
ISI Accession Number IDWOS:000305336300067
Funding AgencyGrant Number
Wong Check She Charitable Foundation
Funding Information:

This study was supported by the Wong Check She Charitable Foundation. This support is from private donations, and no funder's website is available. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

 
DC FieldValue
dc.contributor.authorFung, FKC
 
dc.contributor.authorChan, DW
 
dc.contributor.authorLiu, VWS
 
dc.contributor.authorLeung, THY
 
dc.contributor.authorCheung, ANY
 
dc.contributor.authorNgan, HYS
 
dc.date.accessioned2012-06-06T04:07:11Z
 
dc.date.available2012-06-06T04:07:11Z
 
dc.date.issued2012
 
dc.description.abstractBACKGROUND: Paired-like homeodomain 2 (PITX2) is a bicoid homeodomain transcription factor which plays an essential role in maintaining embryonic left-right asymmetry during vertebrate embryogenesis. However, emerging evidence suggests that the aberrant upregulation of PITX2 may be associated with tumor progression, yet the functional role that PITX2 plays in tumorigenesis remains unknown. PRINCIPAL FINDINGS: Using real-time quantitative RT-PCR (Q-PCR), Western blot and immunohistochemical (IHC) analyses, we demonstrated that PITX2 was frequently overexpressed in ovarian cancer samples and cell lines. Clinicopathological correlation showed that the upregulated PITX2 was significantly associated with high-grade (P = 0.023) and clear cell subtype (P = 0.011) using Q-PCR and high-grade (P<0.001) ovarian cancer by IHC analysis. Functionally, enforced expression of PITX2 could promote ovarian cancer cell proliferation, anchorage-independent growth ability, migration/invasion and tumor growth in xenograft model mice. Moreover, enforced expression of PITX2 elevated the cell cycle regulatory proteins such as Cyclin-D1 and C-myc. Conversely, RNAi mediated knockdown of PITX2 in PITX2-high expressing ovarian cancer cells had the opposite effect. CONCLUSION: Our findings suggest that the increased expression PITX2 is involved in ovarian cancer progression through promoting cell growth and cell migration/invasion. Thus, targeting PITX2 may serve as a potential therapeutic modality in the management of high-grade ovarian tumor.
 
dc.description.naturepublished_or_final_version
 
dc.identifier.citationPLoS One, 2012, v. 7 n. 5, article no. e37076 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0037076
 
dc.identifier.doihttp://dx.doi.org/10.1371/journal.pone.0037076
 
dc.identifier.hkuros199852
 
dc.identifier.isiWOS:000305336300067
Funding AgencyGrant Number
Wong Check She Charitable Foundation
Funding Information:

This study was supported by the Wong Check She Charitable Foundation. This support is from private donations, and no funder's website is available. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

 
dc.identifier.issn1932-6203
2012 Impact Factor: 3.73
2012 SCImago Journal Rankings: 1.512
 
dc.identifier.issue5, article no. e37076
 
dc.identifier.pmcidPMC3352869
 
dc.identifier.pmid22615897
 
dc.identifier.urihttp://hdl.handle.net/10722/148750
 
dc.identifier.volume7
 
dc.languageeng
 
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
dc.publisher.placeUnited States
 
dc.relation.ispartofPLoS One
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.titleIncreased expression of PITX2 transcription factor contributes to ovarian cancer progression
 
dc.typeArticle
 
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