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USP14 activates cell population proliferation. 120 / 128
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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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"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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"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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"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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"However, among these direct targets of TRIM59 identified in this study, PTBP1 silence suppresses the phenotypic transition of PASMCs during PH [31], USP14 promoted the proliferation and migration of vascular smooth muscle cells via mTOR/P70S6K signaling pathway [32], and TPR promoted cellular hypertrophy of vascular smooth muscle cells [33] and enhanced oxidative stress and inflammation [34]."
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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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"Cell Counting Kit-8 (CCK-8) and carboxyfluorescein diacetate succinimidyl ester (CFSE) labelling with flow cytometry analysis were performed to examine cell proliferation, which showed that USP14 depletion significantly decreased the proliferation of PDAC cells, whereas ectopic expression of USP14 led to the opposite phenotype (Fig. 4A, G and S5A–D)."
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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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"Although many reports have shown that highly expressed USP14 promotes cancer cell proliferation via the Wnt/β-catenin pathway and is associated with metastasis [22–24], the substrates and mechanism of USP14 as an oncogene still need to be explored.In this study, through RNA sequencing (RNA-seq) and luciferase assays, we characterized the USP14 regulatory pathway and identified a new substrate of USP14."
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"Therefore, the decrease in the activity of USP14 after treatment with the USP14 inhibitor IU1 and the decrease in the expression of USP14 after the treatment with the USP14-specific siRNA effectively suppressed the proliferation, migration, and wound-healing abilities of gastric cancer cells."
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"The restoration of USP14-WT, in contrast to USP14 C114A, rescued GSC cell proliferation, sphere-forming frequency, and radioresistance (Figure 2E-G), as well as reacquired the ability for intracranial tumor xenograft growth, ultimately diminishing the overall survival of tumor-bearing hosts (Figure 2H)."
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"These findings suggest that USP7 inhibitors may represent a novel approach for treating high-risk NB with MYCN amplification and non-p53 mutations, both as a monotherapy and as an effective adjunct to existing chemotherapy regimens.b-AP15, a small-molecule inhibitor targeting USP14, has been shown to induce apoptosis and inhibit cell proliferation in NB."
eidos
"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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"Then, we also examined the effects of USP14 overexpression on cell proliferation and migration of HASMCs, and the results indicated that overexpression of USP14 significantly promoted the proliferation and migration of HASMCs exposed to PDGF-BB (ESI Fig. 1†).2.4
USP14 regulates expression of VSMCs markers in PDGF-BB-stimulated HASMCs."