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USP8 activates cell population proliferation. 37 / 37
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"The CCK-8 assay showed that USP8 depletion significantly inhibited the proliferation of MCF7 and T47D cells (Figures 3(f) and 3(g))."
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"Our findings indicated that the proliferation, invasion, and stemness of LN229 and T98G cells were markedly suppressed by USP8 inhibition."
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"In addition, USP8 depletion inhibited the proliferation, invasion and stemness of HCC cells and conferred ferroptosis resistance, which effects could be further rescued by beta-catenin overexpression."
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"These results indicated that USP8 could promote tumor proliferation, and invasion of iCCA through ubiquitinating OGT.Post-translational modification (PTM) played a crucial role in iCCA oncogenesis."
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"Furthermore, by overexpressing or silencing USP8, cellular studies indicated that USP8 can directly upregulate the proliferation and metastatic abilities of CSCC cells."
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"In addition, in cervical squamous cell carcinoma (CSCC), USP8 enhanced the proliferation, migration, and invasion of cervical squamous cells, thereby promoting the progression of CSCC [18] ."
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"USP8 expression is higher in ER-positive BC, and upregulation of USP8 mediates cell proliferation and apoptosis and facilitates the cell cycle of BC cells."
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"As USP8 silencing significantly inhibited the PCa cell growth, proliferation, and metastasis and induced apoptosis and suppressed NF-kB signal activation by decreasing EGFR and PI3K, the USP8-specific inhibitor might be a novel therapeutic target to suppress PCa cell growth, proliferation, and metastasis."
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"Depletion of USP8 Inhibits Cell Proliferation, Migration, and Invasion in BC In Vitro."
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"KD of the EGF receptor (EGFR) in human RPE cells inhibits USP8 Tyr717 and Tyr810 phosphorylation, which enables TCHP and AURKA degradation and reverses the serum-induced effects on ciliogenesis and cell proliferation [50]."
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"Elevated levels of USP8 led to cell proliferation, migration, and invasion of CSCC cell lines."
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"Knockdown of USP8 inhibits prostate cancer cell growth, proliferation, and metastasis and promotes docetaxel's activity by suppressing the NF-kB signaling pathway."
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"Finally, USP8 significantly suppresses cellular antiviral responses and enhances SVCV proliferation."
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"Cellular studies showed that USP8 can enhance the proliferation, migration, and invasion abilities of CSCC cells, thereby promoting tumor progression."
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"Mass spectrometry and RNA pull-down assays showed that piR-1742 can directly bind to the hnRNPU protein to form a complex.To the best of our knowledge, this is the first work to elucidate that abundantly expressed piR-1742 might act as a critical mediator in the activation of USP8/MUC12 signaling, hence enhancing the proliferation of RCC cells while also promoting RCC invasion and metastasis."
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"Moreover, we found that USP8 deficiency inhibited pancreatic tumor proliferation and extended overall survival by improving anti-tumor immunogenicity.The most crucial issue in anti-tumor treatment is fixing the therapeutic targets, and increasing studies report that immune checkpoint blockade (ICB) can stimulate the immune system using PD-L1 antibodies, while tumor cells often resist anti-PD-L1 therapy via immune evasion."
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"CCK-8 cell viability tests showed that USP8 can promote tumor cell proliferation, although statistical significance was not achieved (XREF_FIG)."
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"We will provide an overview of corticotroph tumorigenesis in the context of hypothalamic-pituitary-adrenal (HPA) axis regulation with an emphasis on the role of the glucocorticoid receptor in the resistance to the negative feedback of cortisol that occurs in CD, and we will explore the role of epidermal growth factor receptor (EGFR) signaling in ACTH hyper-secretion and corticotroph cell proliferation and the recent discovery of somatic ubiquitin specific peptidase 8 (USP8) mutations in a significant number of patients with sporadic CD with an emphasis on therapeutic implications."
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"However, although overexpressing USP8 in SiHa and SW756 cells enhanced cell proliferation, it did not reach statistical significance according to our data."
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"Indeed, inhibition of USP8 either by its knockdown or synthetic small molecule led to attenuation of variety of receptor tyrosine kinase (RTK) activities, resulting in the inhibition of cell proliferation in gefitinib resistant and -sensitive non small cell lung cancer (NSCLC) cells [XREF_BIBR]."
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"The potential of USP8 as a therapeutic target was also suggested, as inhibitors of USP8 were shown to decrease cell proliferation and ACTH secretion in mouse corticotropinoma‐derived AtT‐20 cells [52]."
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"HuR at the post-transcriptional level increased the level and stability of USP8 mRNA and facilitated translation of USP8 protein, promoting the proliferation, migration, and invasion of NSCLC cells."
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"Knockdown of USP8 inhibited the proliferation, migration, invasion, and cell cycle progression of A549 and H1299 cells, and promoted the apoptosis."
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"Consistent with our previous observations of DUB‐IN‐3, knockout of USP8 significantly suppressed the proliferation, invasion, and stemness of HCC cells (Figure S1, Supporting Information)."
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"Knockdown of USP8 inhibited the proliferation of human lung cancer cells by regulating cell cycle- and apoptosis-related proteins."
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"Although USP8 depletion suppresses cell proliferation in various cancer cells and induces cell death in some cell lines (Islam et al., 2021), whether a direct connection exists between USP8 and ferroptosis remains unknown."
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"Knockdown of USP8 Inhibits the Proliferation and Growth of Lung Cancer Cells."
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"Finally, USP8 could promote tumor proliferation, invasion and stem-like properties of HCC through β-catenin."
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"Knockdown of USP8 significantly inhibited tumor proliferation, invasion, and stem-like properties."
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"The data showed that knockdown of USP8 inhibited the proliferation and promoted the apoptosis of lung cancer cells."
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"Knockdown of USP8 inhibited the proliferation of human lung cancer cells by regulating cyclin- and apoptosis-related proteins."
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"The growth curve showed that the proliferation rate of HTR8/SVneo cells decreased after SCNN1A was silenced, while the overexpression of USP8 significantly increased the proliferation rate ( Supplemen[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"In multiple studies (29–32), the EGFR is a substrate of USP8 deubiquitination, while USP8 has been shown to enhance gastric cancer cell proliferation and metastasis via the PI3K/AKT signaling pathway (30)."
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"Consistent with the results identified above, USP8 WT promoted the proliferation, invasion, and stemness of HCC cells, but the C786A and S716A mutants lost these abilities (Figure 6H–L; Figure S7A–D, Supporting Information)."
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"Ubiquitin-Specific Peptidase 8 Modulates Cell Proliferation and Induces Cell Cycle Arrest and Apoptosis in Breast Cancer by Stabilizing Estrogen Receptor Alpha."
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"It was found that USP8 positively regulated the proliferation and invasion of trophoblast cells and stabilized the ENaC expression on the cell membrane."
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"3.1 Pharmacological USP8 inhibition suppresses GBM cell proliferation."
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