IndraLab

Statements

USP39 activates HYCC1. 31 / 31
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"USP39 promotes HCC cell proliferation and migration by deubiquitinating β-catenin, activating WNT/β-catenin signaling pathway [12]."
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"USP39 stabilizes beta-catenin by deubiquitination and suppressing E3 ligase TRIM26 pre-mRNA maturation to promote HCC progression."
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"The de-acetylation of USP39 by SIRT7 can promote its stability and thereby accelerate HCC cell proliferation and tumorigenesis."
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"In HCC, SIRT7-mediated deacetylation impedes MYST1-facilitated acetylation of USP39, which is a prerequisite for its E3 ligase-induced degradation [55] and accelerates the tumorigenesis of HCC."
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"USP39 promotes the malignant progression of HCC [60, 61] (Fig. 2)."
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"However, the molecular mechanism by which USP39 promotes HCC progression has not been well defined, especially regarding its putative ubiquitination function."
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"USP39 promotes HCC proliferation and migration in vitro."
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"In summary, USP39 significantly promotes the proliferation of HCC cells and enhances their capacity for invasion and metastasis through mechanisms that include the regulation of the Wnt/β-catenin signaling pathway, metabolic reprogramming, and EMT."
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"Moreover, USP39 depletion inhibits HCC cell proliferation and metastasis by promoting ZEB1 degradation."
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"Here, we prove that USP39 promotes HCC cell proliferation and migration by directly deubiquitin beta-catenin, a key molecular of Wnt/beta-catenin signaling pathway whose abnormal expression or activation results in several tumors, following its co-localization with USP39."
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"The mRNA level of USP39 was significantly elevated in HCC."
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"The MTT results showed that silencing USP39 expression significantly inhibited the proliferative ability of HCC cells (Figs."
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"Wound-healing and transwell assays confirmed that USP39 knockdown remarkably suppressed the migration capacities of HCC cells (Fig. 2F–I)."
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"In addition, our previous studies also showed that USP39 promotes HCC progression by the deubiquitination of ZEB1 [19]."
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"The depletion of USP39 could inhibit the proliferation and metastasis of HCC cells [11]."
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"On the other, USP39 promotes the proliferation and invasion of HCC cells by inhibiting splicing of TRIM26, thus affecting the ubiquitin of β-catenin induced by TRIM26."
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"Simultaneously, USP39 knockdown inhibited the proliferation of HCC cells transfected with shTRIM26."
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"USP39 increases proliferation and migration of HCC cells through the Wnt/beta-catenin pathway."
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"Ubiquitin-specific peptidase 39 can promote HCC proliferation by participating in the deubiquitination of SP1[75]."
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"MTT results indicated that knockdown of USP39 reduced the proliferation of HCC cells compared with the control group, while replenishment of USP39 restored the proliferation of HCC cells."
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"Thus, depletion of USP39 could inhibit the proliferation and metastasis of HCC cells."
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"In addition, wound-healing assays showed that silencing USP39 significantly decreased the migration of HCC cells, replenishing USP39 rescued the migration ability impaired by silencing USP39, and the Wnt pathway inhibitor ICG-001 reverted this phenomenon."
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"SIRT7 deacetylates USP39, a deubiquitinating enzyme involved in RNA splicing, promoting its stability and upregulation in HCC."
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"USP39 knockdown also suppressed the shTRIM26-related HCC cell metastasis."
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"These data demonstrated that USP39 increases the proliferation and migration of HCC cells through the Wnt/β-catenin pathway."
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"USP39 has the function of deubiquitination and regulating RNA splicing, and data above has proved USP39 increasing HCC progression through Wnt/β-catenin pathway."
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"Indeed, silencing USP39 expression markedly inhibited the proliferation and metastasis of HCC cells in vitro and in vivo experiments, indicating the potential carcinogenic effect of USP39 in HCC development."
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"SIRT7 promotes HCC development by deacetylation of USP39."
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"Knockdown of USP39 inhibits the growth of HCC cells, potentially through regulating the pre-mRNA splicing of FoxM1 [9] ."
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"The deacetylation of USP39 by SIRT7 promotes the stability and thereby accelerates cell proliferation and tumorigenesis of HCC [10] ."
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"Our data suggested that USP39 activation promotes HCC cell proliferation, and inhibits cell apoptosis.DUBs have recently been identified for their contributions to many types of cancers."
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