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dc.contributor.authorWu, Y-Hen_US
dc.contributor.authorChang, T-Hen_US
dc.contributor.authorHuang, Y-Fen_US
dc.contributor.authorHuang, H-Den_US
dc.contributor.authorChou, C-Yen_US
dc.date.accessioned2014-12-08T15:36:35Z-
dc.date.available2014-12-08T15:36:35Z-
dc.date.issued2014-06-26en_US
dc.identifier.issn0950-9232en_US
dc.identifier.urihttp://dx.doi.org/10.1038/onc.2013.307en_US
dc.identifier.urihttp://hdl.handle.net/11536/24925-
dc.description.abstractBiomarkers that predict disease progression might assist the development of better therapeutic strategies for aggressive cancers, such as ovarian cancer. Here, we investigated the role of collagen type XI alpha 1 (COL11A1) in cell invasiveness and tumor formation and the prognostic impact of COL11A1 expression in ovarian cancer. Microarray analysis suggested that COL11A1 is a disease progression-associated gene that is linked to ovarian cancer recurrence and poor survival. Small interference RNA-mediated specific reduction in COL11A1 protein levels suppressed the invasive ability and oncogenic potential of ovarian cancer cells and decreased tumor formation and lung colonization in mouse xenografts. A combination of experimental approaches, including real-time RT-PCR, casein zymography and chromatin immunoprecipitation (ChIP) assays, showed that COL11A1 knockdown attenuated MMP3 expression and suppressed binding of Ets-1 to its putative MMP3 promoter-binding site, suggesting that the Ets-1-MMP3 axis is upregulated by COL11A1. Transforming growth factor (TGF)-beta (TGF-beta 1) treatment triggers the activation of smad2 signaling cascades, leading to activation of COL11A1 and MMP3. Pharmacological inhibition of MMP3 abrogated the TGF-beta 1-triggered, COL11A1-dependent cell invasiveness. Furthermore, the NF-YA-binding site on the COL11A1 promoter was identified as the major determinant of TGF-beta 1-dependent COL11A1 activation. Analysis of 88 ovarian cancer patients indicated that high COL11A1 mRNA levels are associated with advanced disease stage. The 5-year recurrence-free and overall survival rates were significantly lower (P=0.006 and P=0.018, respectively) among patients with high expression levels of tissue COL11A1 mRNA compared with those with low expression. We conclude that COL11A1 may promote tumor aggressiveness via the TGF-beta 1-MMP3 axis and that COL11A1 expression can predict clinical outcome in ovarian cancer patients.en_US
dc.language.isoen_USen_US
dc.subjectCOL11A1en_US
dc.subjecttumor progressionen_US
dc.subjectovarian carcinomaen_US
dc.titleCOL11A1 promotes tumor progression and predicts poor clinical outcome in ovarian canceren_US
dc.typeArticleen_US
dc.identifier.doi10.1038/onc.2013.307en_US
dc.identifier.journalONCOGENEen_US
dc.citation.volume33en_US
dc.citation.issue26en_US
dc.citation.spage3432en_US
dc.citation.epage3440en_US
dc.contributor.department生物科技學系zh_TW
dc.contributor.department生物資訊及系統生物研究所zh_TW
dc.contributor.departmentDepartment of Biological Science and Technologyen_US
dc.contributor.departmentInstitude of Bioinformatics and Systems Biologyen_US
dc.identifier.wosnumberWOS:000338779300010-
dc.citation.woscount4-
顯示於類別:期刊論文