Abstract
Abstract The presence of the EMT (epithelial-mesenchymal transition) and EndMT (endothelial-mesenchymal transition) demonstrates the extent of phenotypic plasticity in cancers. Previous findings in head and neck squamous cell carcinoma (HNSCC) cells, i.e., VEGF's autocrine-paracrine function and their responsiveness to endostatin, imply that HNSCC cells share some functional characteristics with endothelial cells and suggest the potential for an “epithelial-to-endotheliod transition (EET)”. Such a transition would facilitate HNSCC tumorigenesis by augmenting release of proangiogenic factors and facilitating tumor cell migration and invasion. Consequently, these studies elucidated whether or not an EET occurs in HNSCC cells and tumors, and evaluated cellular parameters to uniquely characterize this epithelial-endotheliod transition. Our results demonstrate that cultured HNSCC cells express a variety of endothelial-specific markers, and assumption of the endotheliod phenotype has functional consequences including uptake of acetylated low density lipoprotein and enhanced invasion and migration. Selective HNSCC cells were also highly responsive to transforming growth factor-β1 and express its auxiliary receptor, endoglin. Furthermore, the EET is not restricted to cultured HNSCC cells per se as tumor cells in resected human HNSCC tumors and proliferating epithelia at the margins of ulcers demonstrate a similar phenotype. These data suggest that, similar to EMT, the EET enhances epithelial cell migration. Also, the regulation of this transition-transient (wound healing) versus sustained (invasive cancers)-impacts clinical outcome. Finally, recognition of the EET as a distinct entity provides impetus for future clinical trials to concurrently assess the antitumorigenic as well as the angiostatic properties of therapeutic agents formally regarded as exclusively angiostatic in scope. 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 3375. doi:10.1158/1538-7445.AM2011-3375
Published Version
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