Epithelial-mesenchymal transition spectrum characterized by an ovarian cancer cell line library defines an aggressive metastable state
Journal
CANCER RESEARCH
Journal Volume
71
Date Issued
2011
Author(s)
Abstract
Abstract Epithelial-mesenchymal transition (EMT) has been implicated to be one of the driving mechanisms of carcinoma progression in many solid tumours, such as breast, colorectal, and ovarian cancer. It explains how carcinoma cells invade and metastasize by transforming an epithelial state via a metastable state to a mesenchymal state. Many studies have addressed the epithelial and mesenchymal states. However, understanding of the metastable state is still limited. In this study, we describe a model system for appraising the spectrum of EMT by using 42 well-characterized ovarian cancer cell lines. Phenotypic EMT characterization reveals 4 subgroups which represent different epithelial-mesenchymal compositions on the EMT spectrum. Genome-wide transcriptional characteristics and recurrent genomic alterations specific for each subgroup are also described. We also demonstrate that this EMT spectrum can be used to refine the analysis of data generated in cell-based functional studies. Ovarian cancer cells harbouring intermediate phenotypes are more migratory, invasive, anoikis resistant, and more spheroidogenic. This ovarian cancer cell line EMT spectrum allows fine tuning of the EMT process by further characterizing the metastable state, which can help reduce heterogeneity. Several candidate genes were applied in a human ovarian carcinoma collection to determine the EMT status by using methods such as quantitative PCR. We conclude that this EMT spectrum library can contribute to the identification of molecular features that serve as predictive diagnostic markers or therapeutic targets associated with EMT. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3437. doi:10.1158/1538-7445.AM2011-3437
SDGs
Publisher
AMER ASSOC CANCER RESEARCH
Type
journal article