IndraLab

Statements

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"Further study demonstrated that USP10 promotes TGF‐β signaling and HCC metastasis through the regulation on the protein abundance of Smad4, but imposing minimal effect on Smad2 and Smad3."
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"Deubiquitinating enzyme USP10 promotes osteosarcoma metastasis and epithelial-mesenchymal transition by stabilizing YAP1."
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"USP10 promotes hepatocellular cancer metastasis by stabilizing Smad4 protein [20]."
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"Deubiquitinase USP10 maintains Cyr61 expression via YAP1 to augment immune escape and metastasis of PAAD."
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"Targeting USP10 by shRNA inhibited CRC proliferation and metastasis, and this effect was reversed by overexpression of NLRP7."
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"In the current study, we found that there was no correlation between expression of TM4SF1 and USP10, S100A12, p53, or Ki67 expression in GC, suggesting that TM4SF1 plays a distinct role in GC invasion and metastasis from those of USP10, S100A12, p53, or Ki67, although they all contribute to cancer invasion and metastasis."
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"As shown in Fig. S5D, the protein levels of USP10 were more abundant and highly correlated with Smad4 expression in tumorous regions compared with that in nontumorous tissues.These results demonstrate that USP10 reinforces the TGF‐β signaling and promotes the metastasis of HCC cells."
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"In order to demonstrate that Smad4 indeed involved in the regulation of USP10 promoting HCC metastasis, we investigated whether Smad4 could rescue the metastasis defect caused by USP10 depletion."
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"Moreover, ablation of USP10 by either shRNAs or USP10 inhibitor Spautin‐1 significantly suppresses the metastasis of HCC cells in vitro and/or in vivo, whereas the reconstitution of Smad4 was able to efficiently rescue this defect, indicating that targeting USP10 could be a novel therapeutic strategy of metastatic HCC displaying high level of Smad4.2 Materials and methods."
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"To extend our in vitro observations concerning USP10’s role in promoting HCC metastasis, we evaluated whether USP10 could promote HCC metastasis in vivo."
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"NLRP7 or USP10 knockdown dramatically inhibited liver metastasis in a mouse model."
33838681
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"Furthermore, we demonstrate that depletion of USP10 or depriving of its catalytic activity with small‐molecule inhibitor Spautin‐1 significantly represses the metastasis of HCC cells in vitro and/or in vivo, whereas the reconstitution of Smad4 was able to efficiently rescue this defect."
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"The current study identified the prometastatic roles of USP10 in HCC and found that USP10 promotes TGF‐β signaling and HCC metastasis by stabilizing Smad4 through the cleavage of proteolytic K48‐linked ubiquitination.5 Conclusions."
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"Deubiquitinating enzyme USP10 promotes hepatocellular carcinoma metastasis through deubiquitinating and stabilizing Smad4 protein."
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"Taken together, these data suggested that depletion of USP10 significantly inhibits HCC metastasis both in vitro and in vivo."
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"HDAC7 promotes NSCLC proliferation and metastasis via stabilization by deubiquitinase USP10 and activation of β-catenin-FGF18 pathway."
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"In addition, the inhibition of USP10 by spautin-1 significantly suppressed the migration and metastasis of HCC."
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"For instance, USP10 promotes tumor metastasis through deubiquitination and stabilization of Smad4 in advanced HCC [8]."
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