作者: Karen D. Cowden Dahl , Richard Dahl , Jessica N. Kruichak , Laurie G. Hudson
DOI: 10.1593/NEO.09942
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摘要: The epithelial-to-mesenchymal transition (EMT) that occurs during embryonic development is recapitulated tumor metastasis. Important regulators of this process include growth factors, transcription and adhesion molecules. New evidence suggests microRNA (miRNA) activity contributes to metastatic progression EMT; however, the mechanisms leading altered miRNA expression cancer remain poorly understood. Importantly, overexpression epidermal factor receptor (EGFR) in ovarian correlates with poor disease outcome induces EMT cells. We report EGFR signaling leads transcriptional repression miR-125a through ETS family PEA3. Overexpression conversion highly invasive cells from a mesenchymal an epithelial morphology, suggesting negative regulator EMT. identify AT-rich interactive domain 3B (ARID3B) as target demonstrate ARID3B overexpressed human cancer. Repression represents novel mechanism for regulating behavior.