IndraLab

Statements



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"Here our studies indicate that DUB3 is crucial to induce EMT through the stabilization of SNAIL1 protein in breast cancer."

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"Dub3 is overexpressed in breast cancer; knockdown of Dub3 resulted in Snail1 destabilization, suppressed EMT and decreased tumour cell migration, invasion, and metastasis."

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"Consistently, Dub3 expression induced a morphologic change indicative of EMT (XREF_FIG), including downregulation of epithelial markers (E-cadherin, Claudin-7 and Occludin) and the upregulation of mesenchymal molecules (N-cadherin and Vimentin) (XREF_FIG, XREF_SUPPLEMENTARY)."

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"DUB3 binds, deubiquitylates and increases cellular levels of the EMT transcription factor SNAIL1 (REF."

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"In fact, DUBs involved in Snail regulation so far are shown to be induced differently, while USP27x is induced by TGF-β; DUB3/USP17L2 seems to play a role in CDK4/6-mediated activation of EMT, whereas OTUB1 is under the transcriptional regulation of oestrogen-related receptor alpha, and USP37 regulation is induced during EMT via the stimulation of the hedgehog signalling pathway."

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"Together, these data indicate that Dub3 can induce EMT (luminal to basal like phenotype conversion) by stabilizing Snail1 in breast cancer cells."

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"Dub3 expression induces EMT."

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"By contrast, ectopic expression of Dub3 induces EMT through an upregulation of Snail."