IndraLab

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"In brief, USP9X promoted the migration and invasion of PANC-1 cells probably by provoking epithelial-mesenchymal transition, and also inhibited apoptosis."

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"USP9X deficiency causes reduced proliferation, cell cycle arrest, and increased apoptosis in HGC-27 and MKN-45 cells, which can be rescued by MTH1 overexpression."

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"Inhibition of USP9X induces apoptosis in FLT3-ITD-positive AML cells cooperatively by inhibiting the mutant kinase through aggresomal translocation and inducing oxidative stress."

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"We speculated that inhibiting USP9X might induce apoptosis in FaDu cells by downregulating Mcl-1 and upregulating Bax protein expression."

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"These results suggest that stabilization of acetylated MCL1 is largely dependent on USP9X and that blockade of USP9X enzymatic activity efficiently induces apoptosis."

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"The involvement of apoptotic cell death is in agreement with other recent studies that have shown that Usp9X loss-of function activates or enhances apoptosis [XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR - XREF_BIBR]."

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"USP9X knockdown promoted FaDu cell apoptosis."

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"ShRNA mediated Usp9x knockdown suppresses 3D growth in PANC1 cells and induces apoptosis in MIAPACA2 cells."

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"Moreover, downregulation of the cellular FADD-like interleukin-1β-converting enzyme-inhibitory protein, which is induced by WP1130, a type of selective USP9X inhibitor that decreases the activity of USP9X, was shown to be regulated by miR-708 through the inhibition of USP9X, which induces the apoptosis of CaSki cells (98)."

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"MCL1 is a member of the antiapoptotic BCL2 family, suggesting that TDRD3-mediated regulation of USP9X attenuates camptothecin (CPT)-induced apoptosis in breast cancer cells [ 97 ]."

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"Inhibiting USP9X might induce apoptosis in FaDu cells by downregulating Mcl-1 and upregulating Bax protein expression."

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"Considering our observations with respect to Bcl-2 family members and IAPs, Usp9X appears to block death-receptor-mediated apoptosis most likely at the level of initiator- as well as effector caspases, involving a combination of factors."

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"revealed that loss of Usp9x increased apoptosis in the hippocampus and medial neocortex at E18.5 and P0 (Usp9x +/Y = 1.1 +/-1.1 cells (n = 9) versus Usp9x -/Y 5.9 +/-5.1 cells, n = 10; p = 0.013)."

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"Furthermore, we demonstrated that knockdown of USP24 but not USP9X could significantly induce growth inhibition and apoptosis of T-ALL cells."

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"In contrast, USP9x knockdown slightly increased apoptosis in IR resistant A172 cells and significantly in Ln229 cells and reduced clonogenic survival after irradiation only on these two cell lines."

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"We proved that USP9X overexpression promoted proliferation and cell cycle and suppressed cell apoptosis in MCL cells."

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"We investigated the role of USP9X in B-ALL and found that USP9X knockdown significantly reduced leukemic cell growth and increased spontaneous apoptosis, thereby improving survival in immunodeficient mice."

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"Although USP9x knockdown reduced Mcl-1 levels and increased apoptosis in A172 cells, USP9x regulated radiosensitivity independently of Mcl-1 in Ln229 cells."

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"Higher concentrations of FAFs markedly inhibited the growth of cells by S-phase arrest and promoted increased tumor cell apoptosis."

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"9–11 For example, USP9X was highly expressed in pancreatic cancer, promoting epithelial mesenchymal transformation and inhibiting cell apoptosis."

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"Together, our results indicate that radiation induced activation of USP9x inhibits Mcl-1 degradation and apoptosis resulting in increased radioresistance."

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"USP9X inhibited cell apoptosis in MCL cells."

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"The results from flow cytometry was proved that USP9X overexpression suppressed cell apoptosis, and USP9X knockdown enhanced cell apoptosis in MCL cells (Z-138 and Jeko-1) (Figure 3A)."

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"Using PANC-1 PC cell line, USP9X was reported to promote tumor metastasis and inhibit tumor apoptosis [ 34 ]."

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"Knockdown of USP9X in pancreatic cells reduced cell growth, migration, and invasion, downregulated EMT markers, and increased apoptosis in vitro and in vivo [158,159,160]."

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"A previous study reported that apoptosis was induced by the inhibition of USP9X at least partly through oxidative stress, which activated DNA damage responses and stress-associated mitogen-activated protein kinase (MAPK) signaling pathways (43)."

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"Furthermore, targeting USP9x in Pbx1 expressing PC cells leads to apoptosis (Liu et al., 2019)."

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"The data implied that USP9X inhibited cell apoptosis in MCL cells."

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"Interference with Usp9x inhibits inflammation and apoptosis of renal tubular epithelial cells."

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"A previous study reported that USP9X overexpression inhibited apoptosis and promoted tumor cell survival (41,57)."

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"The flow cytometry results showed that LPS could promote apoptosis, while Usp9x silencing could reduce the apoptosis of NRK-52E cells (Figure 3F,G)."

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"USP9X knockdown restored the effects of LPS on WI-38 cell proliferation, apoptosis, inflammation, and oxidative stress, but these effects of USP9X knockdown were further abolished by TBL1XR1 overexpression."

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"Flow cytometry found that downregulation of Usp9x significantly suppressed apoptosis, while the upregulation of TLR4 reversed this effect (Figure 5F,G)."

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"Furthermore, the ubiquitin-proteasome system contains an additional deubiquitinase called ubiquitin specific peptidase 9, X-linked (USP9X) that removes poly-ubiquitin chains leading to stabilize Mcl-1 and prevent apoptosis (Schwickart et al., 2010)."

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"Recently, it was reported that USP9X inhibition promotes cell apoptosis in FLT3-ITD AML cells."

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"Usp9X knockdown induces apoptosis, caspase activation and recapitulates effects of CP-d and n-ATF 5-S1."

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"Moreover, USP9X inhibition conferred tumor cell growth disadvantage and enhanced apoptosis in vitro, an effect that occurred in part through its regulation on PEG10."

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"Although both Usp9X and Mcl-1 knockdown elicited some features of apoptosis, broad spectrum caspase inhibition was ineffective in preventing knockdown-induced MPNST cell death suggesting that caspase-independent death pathways were also activated."

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"Similarly, we observed that LPS promoted the expression of Usp9x, and interfered with Usp9x to inhibit the production of inflammatory factors, thereby alleviating apoptosis in renal tubular epithelial cells."

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"Deubiquitinase USP9X promotes cell migration, invasion and inhibits apoptosis of human pancreatic cancer."

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"USP9X was identified to promote proliferation and cell cycle and inhibited cell apoptosis in MCL cells."

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"Downregulation of SOX2 by inhibition of Usp9X induces apoptosis in melanoma."

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"FAM129A inhibited apoptosis and promoted migration and proliferation in human cancers."

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"To determine if Usp9X inhibition induced apoptosis of MPNST cells, we inhibited Usp9X pharmacologically with WP1130 and silenced it by siRNA, as well, in ST88-14 and T265-2c cell lines and examined various biochemical indicators of apoptosis."

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"Usp9x knockdown, as well as inhibition with DUB inhibitor, G9, blocked SOX2 expression, suppressed in vitro colony growth, and induced apoptosis of BRAF-mutant melanoma cells."

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"USP9X overexpression decreased MCF-7 and MDA-MB-231 cell apoptosis."

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"Annexin V-FITC and PI staining combined with flow cytometry showed that USP9X overexpression decreased MCF-7 and MDA-MB-231 cell apoptosis compared with that of the empty vector cells and wild-type cells (both, P<0.05) (Figure 4A–4D)."

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"USP9X gene knockout significantly increased MCF-7 and MDA-MB-231 cell apoptosis compared with cells transfected with negative CRISPR/Cas9 vector (both, P<0.05) (Figure 4A–4D)."

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"The results indicate that USP9X overexpression can decrease breast cancer cell apoptosis, whereas USP9X gene knockout can increase breast cancer cell apoptosis."

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"Here we show that inhibition of the deubiquitinase USP9X by its inhibitor WP1130 or EOAI3402143 (G9) induces apoptosis preferentially in cells transformed by these mutant kinases, including FLT3-ITD-positive AML cell line MV4-11 and primary AML cells."

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"Our previous research found that lncRNA FAF could inhibit apoptosis in ischemia-hypoxia CMs through upregulating FGF9 [ 18 ]."

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"Overexpression of FAF could significantly inhibit cardiomyocytes apoptosis induced by ischemia and hypoxia."

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"Conversely, knockdown of lncRNA FAF could promote apoptosis in ischemia-hypoxia cardiomyocytes."

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"Furthermore, ectopic expression of USP9X prevented c-FLIP downregulation and apoptosis upon combined treatment."

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"Inhibition of USP9X Downregulates JAK2-V617F and Induces Apoptosis Synergistically with BH3 Mimetics Preferentially in Ruxolitinib-Persistent JAK2-V617F-Positive Leukemic Cells."

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"Inhibition of the deubiquitinase USP9x induces pre-B cell homeobox 1 (PBX1) degradation and thereby stimulates prostate cancer cell apoptosis."

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"Inhibition of USP9X by WP1130 downregulates MCL1 protein , inducing apoptosis in CML cell lines [ 103 ] ."

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"USP9X inhibition promotes radiation induced apoptosis in non small cell lung cancer cells expressing mid-to-high MCL1."

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"USP9X promotes tumor cell survival and inhibits apoptosis by de-ubiquitinating and stabilizing MCL1."

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"Both knockdown and chemical inhibition of USP9X have been shown to efficiently promote cancer cell apoptosis."

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"Knockdown of USP9X inhibited cell proliferation and cell cycle progression and increased apoptosis."

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"USP9x is also found to deubiquitinate and stabilize pre-B-cell leukemia homeobox-1 (PBX1) in advanced prostate cancer (PCa), thereby abrogating apoptosis and conferring chemoresistance to doxorubicin or cisplatin [208]."

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"45 Interestingly, inhibition of the deubiquitinase USP9X, which cleaves various Ub chains, including K48 and K63 linkages, induced apoptosis preferentially in cells transformed by the ITD mutant and decreased the downstream signaling event."

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"Overexpressing LncRNA FAF can inhibit cardiomyocyte apoptosis induced via ischemia and hypoxia."

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"A novel long noncoding RNA FAF inhibits apoptosis via upregulating FGF9 through PI3K and AKT signaling pathway in ischemia-hypoxia cardiomyocytes."

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"As inhibition of USP9X resulted in caspase 3 and caspase 8 activation and increased the rates of apoptosis, USP9X might promote cell survival by inhibiting apoptosis in glioma cells."

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"Since suppression of Usp9X significantly enhances apoptosis induced by ABT263, we determined the effects of ABT263 on Usp9X and Bag3 protein levels."