IndraLab

Statements

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"For instance, USP39 promotes colorectal cancer growth and metastasis through the Wnt and beta-catenin pathway [XREF_BIBR]."
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"USP39 protein promotes the growth and metastasis of colorectal cancer mainly through the Wnt/β-catenin pathway [8] ."
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"Thus, depletion of USP39 could inhibit the proliferation and metastasis of HCC cells."
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"Knockout of USP39 can inhibit tumor genesis, induce cell apoptosis, and inhibit lung adenocarcinoma cell metastasis [13]."
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"The results showed that USP39 knockdown led to an obvious reduction in tumor metastasis, while TRIM26 downregulation enhanced the tumor metastasis and reversed the reduction of shUSP39-related cell metastasis and the number of nodules in the lung (Fig. 8G, H)."
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"USP39 contributes to CRC growth and metastasis through the Wnt/β-catenin pathway."
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"USP39 promotes colorectal cancer growth and metastasis through the Wnt and beta-catenin pathway."
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"USP39 knockdown also suppressed the shTRIM26-related HCC cell metastasis."
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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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"For example, Yuan et al. [13] found that USP39 is upregulated in NSCLC tissues, and USP39 knockout can inhibit the growth and metastasis of NSCLC cells."
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"Deubiquitinating enzyme USP39 promotes the growth and metastasis of gastric cancer cells by modulating the degradation of RNA-binding protein RBM39."
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"The depletion of USP39 could inhibit the proliferation and metastasis of HCC cells [11]."
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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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"Together, these data demonstrate that USP39 knockdown inhibits the metastasis of lung cancer cells in vivo and in vitro."
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"Moreover, USP39 depletion inhibits HCC cell proliferation and metastasis by promoting ZEB1 degradation."
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