T. King, M. Key, J. Clifford
Nov 12, 2011
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Molecular Cancer Therapeutics
Abstract
Fusarochromanone (FC-101a) has been identified as a potential, novel anti-cancer compound. Several studies revealed that FC-101a is an inhibitor of many human cancer cell lines, increases apoptosis of melanoma cell lines and significantly reduces tumor growth in mice. The long-term goal of this project is to elucidate how FC-101a inhibits cancer cell growth by identifying its molecular target(s). In this study, we used DNA microarray analysis and realtime PCR to identify genes that are differentially-expressed in response to FC-101a treatment in yeast and human bladder cancer cells. We hypothesize that changes in gene expression in response to FC-101a treatment will elucidate cellular mechanisms by which FC-101a inhibits cancer cell growth. Our study includes human cancer cell lines as a model system and budding yeast as a model organism to identify cellular pathways that are responsive to FC-101a treatment in multiple eukaryotic cell types. In this study, we have determined that among human skin, breast, prostate and bladder cancer cell lines, bladder cancer cells are the most sensitive to FC-101a treatment. Thus, we performed DNA microarray analysis using human bladder carcinoma cells treated with FC-101a for 24, 48 and 72 hours and yeast cells treated with FC-101a for 20 minutes. We identified hundreds of genes that are highly expressed and greater than two-fold up-regulated or down-regulated in FC-101a-treated cells compared with untreated cells. Of these FC-101a-responsive genes common to yeast and human bladder cancer cells, a majority of these genes regulate apoptosis, metabolic pathways, cell cycle progression, DNA replication, cell signaling and DNA recombination and repair. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2011 Nov 12-16; San Francisco, CA. Philadelphia (PA): AACR; Mol Cancer Ther 2011;10(11 Suppl):Abstract nr A35.