IndraLab

Statements

USP39 activates FAM126A. 14 / 14
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"Simultaneously, USP39 knockdown inhibited the proliferation of HCC cells transfected with shTRIM26."
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"SIRT7 promotes HCC development by deacetylation of USP39."
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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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"Here, we prove that USP39 promotes HCC cell proliferation and migration by directly deubiquitin β-catenin, a key molecular of Wnt/β-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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"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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"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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"The MTT results showed that silencing USP39 expression significantly inhibited the proliferative ability of HCC cells (Figs."
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"Moreover, USP39 depletion inhibits HCC cell proliferation and metastasis by promoting ZEB1 degradation."
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"The depletion of USP39 could inhibit the proliferation and metastasis of HCC cells [11]."
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"Thus, depletion of USP39 could inhibit the proliferation and metastasis of HCC cells."
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"USP39 promotes HCC proliferation and migration in vitro."
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"USP39 stabilizes β-catenin by deubiquitination and suppressing E3 ligase TRIM26 pre-mRNA maturation to promote HCC progression."
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"USP39 knockdown also suppressed the shTRIM26-related HCC cell metastasis."
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