| RUNX3 protein is overexpressed in human epithelial ovarian cancer. | |
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MedLine Citation:
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PMID: 18937968 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVE: RUNX family genes, including RUNX3, are developmental regulators that are important in human cancers. The purpose of this study was to evaluate expression and oncogenic potential of RUNX3 in ovarian carcinoma. METHODS: Immunohistochemical staining was performed on 60 malignant, 14 borderline, and 5 normal ovarian specimens. Correlation between RUNX3 expression with tumor histology was performed. RUNX3 expression was evaluated by quantitative real-time polymerase chain reaction (QRT-PCR) in microdissected normal and malignant epithelial ovarian tissues. Cell proliferation and viability studies were performed on cells expressing RUNX3 by lentiviral infection and cells with silenced RUNX3 expression by siRNA. RESULTS: RUNX3 expression by immunohistochemistry was higher in serous ovarian carcinomas versus normal ovarian epithelium (P<0.001). Immunofluorescent staining confirmed upregulation of cytoplasmic RUNX3 in ovarian cancer cell lines and tissues. QRT-PCR showed higher RUNX3 mRNA expression in microdissected borderline and malignant ovarian tumor tissues compared with the normal ovarian surface epithelial cells (HOSE) (P=0.006 and P=0.023). Forced RUNX3 expression by lentiviral gene delivery in ovarian cancer cells, SKOV3, that initially showed undetectable RUNX3 expression, resulted in increased cell viability (P=0.043). Silencing RUNX3 expression by siRNA transfection into ovarian cancer cells, OVCAR429, initially expressing high levels of endogenous RUNX3 resulted in a decrease in proliferation (P=0.021). CONCLUSION: These results suggest that RUNX3 has a role in cell proliferation and viability in ovarian cancer. |
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Authors:
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Nicole S Nevadunsky; John S Barbieri; Joseph Kwong; Melissa A Merritt; William R Welch; Ross S Berkowitz; Samuel C Mok |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2008-10-19 |
Journal Detail:
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Title: Gynecologic oncology Volume: 112 ISSN: 1095-6859 ISO Abbreviation: Gynecol. Oncol. Publication Date: 2009 Feb |
Date Detail:
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Created Date: 2009-01-19 Completed Date: 2009-01-26 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0365304 Medline TA: Gynecol Oncol Country: United States |
Other Details:
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Languages: eng Pagination: 325-30 Citation Subset: IM |
Affiliation:
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Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, Laboratory of Gynecologic Oncology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Cell Growth Processes
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physiology Cell Line Core Binding Factor Alpha 3 Subunit / biosynthesis*, genetics Cytoplasm / metabolism Female Gene Expression Regulation, Neoplastic Gene Silencing Humans Immunohistochemistry Ovarian Neoplasms / genetics, metabolism*, pathology Ovary / metabolism, physiology RNA, Messenger / biosynthesis, genetics RNA, Small Interfering / genetics Up-Regulation |
| Grant Support | |
ID/Acronym/Agency:
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P50CA165009/CA/NCI NIH HHS; R33CA103595/CA/NCI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Core Binding Factor Alpha 3 Subunit; 0/RNA, Messenger; 0/RNA, Small Interfering; 0/Runx3 protein, human |
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