Document Detail


RUNX3 protein is overexpressed in human epithelial ovarian cancer.
MedLine Citation:
PMID:  18937968     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
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:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2008-10-19
Journal Detail:
Title:  Gynecologic oncology     Volume:  112     ISSN:  1095-6859     ISO Abbreviation:  Gynecol. Oncol.     Publication Date:  2009 Feb 
Date Detail:
Created Date:  2009-01-19     Completed Date:  2009-01-26     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0365304     Medline TA:  Gynecol Oncol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  325-30     Citation Subset:  IM    
Affiliation:
Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, Laboratory of Gynecologic Oncology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
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MeSH Terms
Descriptor/Qualifier:
Cell Growth Processes / 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:
P50CA165009/CA/NCI NIH HHS; R33CA103595/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Core Binding Factor Alpha 3 Subunit; 0/RNA, Messenger; 0/RNA, Small Interfering; 0/Runx3 protein, human

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