IndraLab

Statements



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"Importantly, expression of WT, but not mutant USP27X, prevented the proliferation defects caused by depletion of endogenous USP27X (XREF_FIG)."

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"Importantly, expression of WT, but not mutant USP27X, prevented the proliferation defects caused by depletion of endogenous USP27X."

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"Furthermore, USP27 or SETD3 knockdown inhibits cell proliferation, cell migration and tumorigenesis, while overexpression of SETD3 in USP27-deficient HCC cells could restore cell viability."

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"Knockdown of USP27 by short hairpin RNA (shRNA) accelerated the degradation of SETD3 and blocked cell proliferation."

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"To determine how USP27X promotes cancer cell proliferation, we first performed immunoblots comparing the expression of several cell signaling molecules."

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"The observation that USP27 promotes cell cycle progression and cell proliferation prompted us to imagine that depletion of USP27 expression might suppress tumor progression."

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"Herein, we demonstrate that USP27 regulates Cyclin E abundance to accelerate cell cycle progression, cell proliferation, and tumor cell growth as well."

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"These results suggest that USP27X is required to support cancer cell proliferation as opposed to regulating cell death."

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"Furthermore, cell proliferation was also remarkably reduced in the combination of USP27 knockdown and 5-FU treatment, whereas overexpression of USP27 or addition of Cyclin E in USP27 knockdown cells could raise cell proliferation."

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"Expression of WT-USP27X on its own led to slightly increased proliferation, whereas expression of the C285S mutant led to slightly reduced proliferation."

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"Furthermore, evidence from in vitro and in vivo studies revealed that depletion of USP27 inhibited HCC cell proliferation, invasion, metastasis and tumorigenesis, and that overexpression of SETD3 rescued this phenotype."

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"Our data showed that USP27 promotes cell proliferation and migration."

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"Stabilization of SETD3 by deubiquitinase USP27 enhances cell proliferation and hepatocellular carcinoma progression."

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"SETD3 reverses the USP27 knockdown mediated blockade of cell proliferation."

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"The finding that USP27–SETD3 axis elevates the cell proliferation and migration prompted us to imagine that they might be upregulated in hepatocellular carcinoma."

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"Upregulation of USP27 in hepatocellular carcinoma patients leads to elevated SETD3 expression and increased cell proliferation, invasion, migration and tumorigenesis."