【摘 要】
：
Epithelial tumor cells that have undergone epithelial-to-mesenchymal transition (EMT) are typically metastasis prone and drug resistant and contribute to a poor clinical outcome.Here,we show that phos
【机 构】
：
Division of Pulmonary and Critical Care Medicine,Mayo Clinic,Rochester,MN,USA;Thoracic/Head and Neck
【出 处】
：
8th IUPAP International Conference on Biological Physics(第八届
论文部分内容阅读
Epithelial tumor cells that have undergone epithelial-to-mesenchymal transition (EMT) are typically metastasis prone and drug resistant and contribute to a poor clinical outcome.Here,we show that phosphatidylinositol 3-kinase (PI3K)-targeted therapy suppressed metastasis in a mouse model of Kras/Tp53-mutant lung adenocarcinoma that develops metastatic disease because of high expression of ZEB1, a transcriptional driver of EMT.ZEB1 activated Pl3K by de-repressing miR-200 targets (AREG, BTC, and GATA6) that stimulated an EGFR/ERBB2 autocrine loop and by de-repressing a miR-200 and miR-183 target, friend-of-GATA 2 (FOG2),that enhanced GATA3-induced expression of the p110α catalytic subunit.Loss-of-function studies showed that FOG2, p110α, and RHEB were required for the invasive and metastatic propensities of tumor cells.
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