IndraLab

Statements



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"Functionally, USP14 overexpression reduced apoptosis and increased cell migration, invasion, and EMT in vivo and ex vivo."

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"Notably, USP14 can also directly deubiquitinate and activate PI3K and lidocaine can inhibit the expression of USP14 and the activation of PI3K/AKT in HCC, and significantly inhibit the proliferation, [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"More recently, Hang et al. reported that USP14 promoted cell proliferation, invasion, and migration and prevented apoptosis in vitro [34]."

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"In vitro experiment revealed that USP14 depletion markedly inhibited cell growth, cisplatin resistance, invasion and migration capabilities of HNSCC cells."

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"To investigate the molecular mechanism by which USP14 promoted proliferation and invasion in ESCC cells, we examined the effects of USP14 on the activation of the Wnt and beta-catenin signaling pathway."

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"Overexpressing USP14 reduced apoptosis and promoted EC cell migration and invasion."

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"By detecting cell migration and invasion by Transwell assay, it was found that USP14 knockdown reduced EC cell migration and invasion (Figure 4E)."

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"Furthermore, administration of the IU1-47 small molecule or siRNA inhibition of USP14 was demonstrated to significantly decrease lung cell proliferation, migration, and invasion."

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"The results indicated that knockdown of BACH1 protein or treatment with the HO-1 inhibitor ZnPPIX significantly reduced the cell invasion induced by USP14 overexpression ( Fig. 6 A–C)."

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"In addition, IU1, a small-molecule inhibitor of USP14, accelerated the degradation of a subset of proteasome substrates and suppressed cell proliferation, migration, and invasion in lung cancer and cervical cancer."

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"By engaging in interaction and deubiquitination of BACH1, USP14 influences heme metabolism and contributes to the invasiveness of ovarian cancer cells."

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"Moreover, USP14 can promote the proliferation and invasion of HNSCC both in vivo and in vitro.Ubiquitin-specific peptidase 4 (USP4) has been identified to deubiquitinate K63-linked ubiquitin conjugates from TNF receptor-associated factor 2 (TRAF2), TNF receptor associated factor 6 (TRAF6), and TGF-beta activated kinase 1 (TAK1) and stabilizes molecules by deubiquitinating K48-linked ubiquitination [63]."

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"In one study, USP14 was found to promote GC cell proliferation, invasion, and migration by stabilizing the EMT protein vimentin."

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"Overexpression of USP14 inhibits I-κB and increases NF-κB phosphorylation while increasing cancer cell migration, invasion, and EMT (108)."

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"Genetic or pharmaceutical inhibition of USP14 has been shown to significantly decrease the proliferation, migration, and invasion of lung cancer cells."

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"Overexpression of USP14 could enhance proliferation, prevent apoptosis and promote invasion and migration of PDAC cells."

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"Moreover, the USP14 overexpression could enhance the proliferation, migration, and invasion and also reduce apoptosis of PDAC cells via regulating the expression of cyclin D1, PCNA, and E-cadherin [25]."

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"Transwell assays and wound healing assays showed that the USP14 depletion reduced the migration and invasion of PDAC cells, whereas USP14 overexpression enhanced these abilities (Fig. 5A, B, F, G and S6A–D)."

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"USP14 knockdown in SCC47 and SCC090 cells inhibited collective invasion and abrogated the invasive phenotype induced by CDK4 depletion (figure 5G–J and online supplemental figure 7I–L)."