Abstract
Abstract Clear cell ovarian cancer (CCOC) is the second most common subtype of ovarian cancer after serous ovarian cancer. CCOC is more resistant to standard chemotherapy and has a poorer prognosis than serous and endometrioid histotypes. We attempted to identify genes that are responsible for the aggressive behavior of CCOC and could be potential therapeutic targets using genomic and expression profilings. To identify gene amplification, genome-wide DNA copy number alterations were measured in 13 CCOC cell lines using high-resolution oligonucleotide array CGH (Agilent 105k Human Genome CGH Microarray). GISTIC analysis identified 16 amplified regions containing 391 genes. After comparison to our database of differentially expressed genes between human CCOC specimens and normal ovarian surface epithelium specimen (Affymetrix U133 Plus 2.0 microarrays), 45 of the amplified genes showed mRNA overexpression in CCOC specimens. Among the 45 genes, fibroblast growth factor receptor 3 (FGFR3) was amplified in 9/13 CCOC cell lines and was overexpressed (12.9 folds) in CCOC specimens. Analysis using PathwayStudio software identified FGFR3 mediated pathways for cell migration and cell proliferation. Knockdown of FGFR3 by transfection with FGFR3 specific shRNAs suppressed cell migration in KOC-7c and HAC-2 cells. Moreover, knockdown of FGFR3 also suppressed anchorage-dependent cell proliferation of KOC-7c and HAC-2 cells. The results from the present study therefore suggested that FGFR3 may promote metastasis and growth of cancer cells and may serve as a potential target gene for treatment of human clear cell ovarian cancer. Citation Format: Tsun Yee Tsang, Gayatry Mohapatra, Hiroaki Itamochi, Samuel C. Mok, Michael J. Birrer. Identification of FGFR3 as a potential therapeutic target gene for human clear cell ovarian cancer by global genomic analysis. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1528. doi:10.1158/1538-7445.AM2014-1528
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