mics fully suppressed the effects of OSM. Notably, РHMGA2 as an early embryonic gene is highly expressed in undifferentiated Рproliferating cells during embryogenesis and es silent in adult tissues. РConversely, the expression of let-7 is barely detectable in embryonic stages but Рupregulated at the end of embryonic development. We speculate that the transient Рactivation of let-7-HMGA2 axis may act as an ic switch to trigger РOSM-induced EMT. Knockdown of HMGA2 markedly reversed the EMT phenotype, Рrepressed invasive capability of breast cancer cells and restored the expression of РmiR-200, which was downregulated later under OSM stimulation. These data suggest Рthat the dynamic alterations of let-7 and HMGA2 not only elicit OSM-induced EMT, Рbut also impact the expression of miR-200. Р 6
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