IndraLab

Statements

USP10 activates FAM126A. 10 / 10
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"The suppression of USP10 by either shRNAs or catalytic inhibitor Spautin-1 significantly inhibited the migration of HCC cells, whereas the reconstitution of Smad4 was able to efficiently rescue this defect."
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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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"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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"Taken together, these data suggested that depletion of USP10 significantly inhibits HCC metastasis both in vitro and in vivo."
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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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"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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"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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"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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"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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"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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