IndraLab

Statements


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"16 Although USP11 plays a critical role in HCC progression, and our earlier research established that USP11 inhibits autophagy through targeting ERK/mTOR pathway to promote HCC metastasis, 16 the mechanisms of USP11 in HCC glycolysis remain poorly understood.Various biological processes, including hypoxia, are related to protein homeostasis, which maintained by post‐translational modification."

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"The E2F1 and USP11 positive feedback loop promotes hepatocellular carcinoma metastasis and inhibits autophagy by activating ERK and mTOR pathway."

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"Moreover, a recent study has also reported that depletion of USP11 homolog H34C03.2 in Caenorhabditis elegans triggers autophagy hyperactivation and alleviates human Aβ aggregation-induced paralysis (Basic et al, 2021)."

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"Therefore, further studies are warranted in this regard.Multiple studies suggest that mTOR may be a central regulator of autophagy.100 101 Moreover, some studies have shown that USP11 can inhibit cell autophagy through the ERK/mTOR pathway, which promotes the proliferation and metastasis of cancer cells."

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"Moreover, E2F1 and USP11 inhibited autophagy by regulating ERK and mTOR pathway."

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"103 However, whether USP11 can inhibit autophagy through the ERK/mTOR pathway and play a key role in BC development needs further exploration."

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"Here, we show that the deubiquitinase USP11 restricts autophagy and that knockout (KO) of USP11 in mammalian cells results in elevated autophagic flux."

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"Taken together, these results indicate that the E2F1 and USP11 signal axis promotes HCC proliferation and metastasis and inhibits autophagy, which provides an experimental basis for the treatment of HCC."

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"We also demonstrate that depletion of the USP11 homolog H34C03.2 in Caenorhabditis elegans triggers hyperactivation of autophagy and protects the animals against human β-amyloid peptide 42 aggregation-induced paralysis."