IndraLab

Statements



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"Recently, researches have revealed USP14 enhances cisplatin resistance through affecting Akt and ERK signaling pathways and accelerates cell proliferation and migration in GC."

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"To explore the underlying mechanism by which USP14 promotes cell proliferation in LNcap cells, we monitored the cell cycle progression of each group exposed to various concentrations of IU1 (25, 50, 100muM) and found that inhibition of USP14 activity dramatically induced G0/G1 cell cycle arrest at different time points (0, 6, 12, 24, 48h) (XREF_FIG)."

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"USP14 has been reported to be overexpressed in LUAD and promote proliferation through the accumulation of β-catenin."

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"Knockdown of USP14 in HASMCs suppressed PDGF-BB-induced proliferation and migration of HASMCs."

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"We found that USP14 inhibition by shRNA significantly suppressed the proliferation of MDA-MB-231, MDA-MB-453, MDA-MB-468, HCC1937, and MCF7 breast cancer cell lines; however USP14 knockdown did not affect the proliferation of T47D cells, which could be related to the fact that these cells express very high levels of ER and very low levels of AR."

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"Additionally, USP14 depletion and its inhibitor IU1 significantly inhibited cell proliferation, migration, and angiogenesis in HCC, suggesting that USP14 might be a potential therapeutic target for HCC."

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"Recently , researches have revealed USP14 enhances cisplatin resistance through affecting Akt / ERK signaling pathways and accelerates cell proliferation and migration in GC ( Fu et al ., 2018 ; Han K.H ."

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"USP14 was overexpressed in many cancers and promoted tumor cell proliferation through enhancing beta-catenin accumulation and inhibiting Bcl-xl-mediated cell apoptosis 11."

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"USP14 promotes NSCLC cell proliferation, which may be associated with beta-catenin accumulation."

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"These data suggest that knockdown of USP14 inhibits the proliferation and tumorigenesis in ESCC cells by suppressing and inhibiting the Wnt and beta-catenin signaling pathway."

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"Both genetic knockdown and pharmacological inhibition of USP14 inhibits the proliferation and induces the apoptosis of AR-positive breast cancer cells (Table 2)."

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"As reported previously, cell proliferation was reduced by FASN or USP14 knockdown, respectively [7,30]."
| PMC

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"These results indicated that individual inhibition of USP14 and FASN mildly reduced cancer cell proliferation, but contrary to our expectation, no synergistic effect was confirmed when both were inhibited."
| PMC

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"Taken together , it suggests that USP14 inhibition suppresses cell proliferation at least in part by inducing cell apoptosis ."

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"Overexpression of USP14, which is a novel regulator of AR (Figure 5), accelerates the proliferation of PC cells through the deubiquitination and inhibition of the degradation of AR in androgen-responsive PC cells."

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"This observation may be due to enhanced apoptotic cell death by apoptosis that counters the increase of total population when treated with b-AP15, therefore causing an overall suppression of cancer ce[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Moreover, knockdown of USP14 by shRNA also inhibited the proliferation and migration of OSCC cells in vitro."

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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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"Inhibition of USP14 suppresses the proliferation of breast cancer."

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"USP14 knockdown or treatment with USP14 inhibitor IU1 induced G0/G1 cell cycle arrest and suppressed cell proliferation in AR-positive and ER-negative breast cancer cells and androgen responsive prost[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Using MTT assays, colony formation analyses, flow cytometry assays, and cell invasion and migration assays, we found that knockdown of USP14 attenuated proliferation, induced apoptosis and restrained invasion and migration of PDAC cells."

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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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"We found that (i) USP14 could bind to AR, and additionally, both genetic and pharmacological inhibition of USP14 accelerated the ubiquitination and degradation of AR; (ii) downregulation or inhibition of USP14 suppressed cell proliferation and colony formation of LNcap cells and, conversely, overexpression of USP14 promoted the proliferation; and (iii) reduction or inhibition of USP14 induced G0/G1 phase arrest in LNcap prostate cancer cells."

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"Non small cell lung cancer (NSCLC) tissues overexpress USP14, which promotes tumor cell proliferation and is associated with shorter overall survival time."

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"Given that USP14 is expressed in both androgen responsive and androgen-irresponsive prostate cancer cells and that both pharmacological and genetic inhibition of USP14 inhibited the proliferation of androgen responsive LNcap cells, we next tested whether USP14 plays the same role in androgen-irresponsive prostate cancer cells."

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"Inhibition or depletion of USP14 inhibited the proliferation and survival of HNSCC cells."

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"The above results suggested USP14 promotes HCC cell proliferation partially in a HIF1-α-dependent manner."

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"USP14 positively regulates the proliferation of androgen responsive prostate cancer cells."

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"USP14 depletion or its specific inhibitor IU1 treatment decreased cell proliferation , invasion , migration , and Vascular Mimicry ( VM ) formation even under hypoxia conditions in HCC cell lines ."

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"In lung adenocarcinoma, overexpression of USP14 promoted cell proliferation through the accumulation of beta-catenin."

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"19 In addition , small USP14 inhibitors , such as WP1130 , b-AP15 , AC17 , and pyrithione , could dramatically suppressed cell proliferation and promoted apoptosis in various malignancies.9 , 20 , 21 , 22 , 23 , 24 However , we did not observe any disturbed biological process , such as cell cycle progression , cell proliferation , and apoptosis , in USP14-deficient GC cells , although silencing of USP14 dramatically inhibited Akt and ERK signaling pathways ."

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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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"In addition, b-AP15, a novel inhibitor of USP14, selectively blocks the deubiquitylating activity of USP14, decreases viability and inhibits proliferation of MM cells, which is associated with growth [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"USP14 or ATF2 knockdown inhibited HG-induced HRMECs proliferation, migration, and tube formation."

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"Overexpression of USP14 promotes cell proliferation and migration, while down-regulation induces cell apoptosis and inhibits cell proliferation, migration, and invasion."

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"Conversely, overexpression of USP14 induced increases in the protein level of cyclinD1and CDK6/4/2, the inactivation of Rb, and decreases in the expression of p27 and p15 (XREF_FIG), and led to increased proliferation of LNcap cells (XREF_FIG)."

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"Growth curves analysis showed that USP14 depletion and its inhibitor IU1 inhibited cell proliferation under normoxia and hypoxia conditions (Fig. 4A, B)."

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"The results showed that the expression of USP14 increases significantly in non-small cell lung cancer (NSCLC) tissue, particularly in lung adenocarcinoma tissues, and over-expression of USP14 promotes tumor cell proliferation."

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"USP14 increases cell proliferation in HCC cell lines."

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"These data suggested that knockdown of USP14 prevented PDGF-BB-induced proliferation, migration, and phenotypic modulation of HASMCs via inhibiting the mTOR/P70S6K signaling pathway."

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"Additionally, both genetic and pharmacological inhibition of USP14 significantly suppressed cell proliferation in AR responsive breast cancer cells by blocking G 0 / G 1 to S phase transition and inducing apoptosis."

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"We found that USP14 knockdown resulted in inhibition of cell proliferation in all six cell lines ( Figs ."

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"Over-expression of USP14 was associated with poor prognosis in NSCLC patients and promoted tumor cell proliferation, which suggests that USP14 is a tumor promoting factor and a promising therapeutic target for NSCLC."

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

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"Over-Expression of Deubiquitinating Enzyme USP14 in Lung Adenocarcinoma Promotes Proliferation through the Accumulation of beta-Catenin."

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"We found that the expression of USP14, Ki67, and HIF1-α, which promote proliferation, were decreased in the shUSP14 group (Fig. 7G)."

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"Ubiquitin specific protease 14 (USP14) promotes proliferation and metastasis in pancreatic ductal adenocarcinoma."

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"It was found that the administration of 6-Gingerol decreased the expression of USP14, greatly increased the number of autophagosomes, reactive oxygen species (ROS) and iron concentration, decreased the survival and proliferation rate of A549 cells, and significantly decreased tumor volume and weight."

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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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"AKT induced phosphorylation of USP14 may also promote tumor cell proliferation by regulating global proteomic turnover [XREF_BIBR]."