Functional characterization of a panel of high-grade serous ovarian cancer cell lines as representative experimental models of the disease.

2016 
// James Haley 1 , Sunil Tomar 1 , Nicholas Pulliam 1 , Sen Xiong 1 , Susan M. Perkins 2 , Adam R. Karpf 3 , Sumegha Mitra 1, 4 , Kenneth P. Nephew 1, 5, 6 , Anirban K. Mitra 1, 5, 7 1 Medical Sciences Program, Indiana University School of Medicine, Bloomington, IN 47405, USA 2 Department of Biostatistics, Indiana University, Indianapolis, IN 46202, USA 3 Eppley Institute and Fred and Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198, USA 4 Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN 46202, USA 5 Indiana University Melvin and Bren Simon Cancer Center, Indianapolis, IN 46202, USA 6 Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA 7 Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN 46202, USA Correspondence to: Anirban K. Mitra, email: anmitra@indiana.edu Keywords: ovarian cancer, migration, invasion, proliferation, clonogenicity Received: January 27, 2016      Accepted: April 10, 2016      Published: April 27, 2016 ABSTRACT Genomic analysis of ovarian cancer cell lines has revealed a panel that best represents the most common ovarian cancer subtype, high-grade serous ovarian cancer (HGSOC). However, these HGSOC-like cell lines have not been extensively applied by ovarian cancer researchers to date, and the most commonly used cell lines in the ovarian cancer field do not genetically resemble the major clinical type of the disease. For the HGSOC-like lines to serve as suitable models, they need to be characterized for common functional assays. To achieve that objective, we systematically studied a panel of HGSOC cells CAOV3, COV362, Kuramochi, OVCAR4, OVCAR5, OVCAR8, OVSAHO and SNU119 for migration, invasion, proliferation, clonogenicity, EMT phenotype and cisplatin resistance. They exhibited a range of efficacies and OVCAR5, OVCAR8 and Kuramochi were the most aggressive. SNU119 and OVSAHO cells demonstrated the lowest functional activities. Wide differences in expression of EMT markers were observed between cell lines. SNU119 were the most epithelial and OVCAR8 had the most mesenchymal phenotype. COV362 was the most resistant to cisplatin while CAOV3 was the most sensitive. Taken together, our systematic characterization represents a valuable resource to help guide the application of HGSOC cells by the cancer research community.
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