IndraLab

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USP8 activates Neoplasms. 31 / 31
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"Studies have shown that USP8 can promote migration and invasion in tumors."
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"USP8 promotes cancer progression and extracellular vesicle-mediated CD8 + T cell exhaustion by deubiquitinating the TGF-beta receptor TbetaRII ."
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"Usp8 ;Vil-Cre mice developed fewer and smaller tumors in the colon than Usp8 mice, indicating that Usp8 deficiency in IECs inhibits the colorectal tumorigenesis and tumor progression (Fig. 2 B–D)."
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"In order to get an insight into the mechanism through which USP8 enhance tumor progression, we analyzed the relationship between USP8 expression and patient survival in 20-different human cancers provided by OncoRank (http://www.oncolnc.org)."
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"In vivo, silencing lncRNA SNHG12 mitigated tumor growth and immune escape, decreased PD-L1 and USP8 expression, and increased PD-L1 ubiquitination level in tumor tissues."
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"Taken together, our results suggest that deletion of Usp8 significantly inhibits colorectal and lung tumorigenesis and tumor progression accompanied by increased lipid peroxidation in tumors."
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"The results showed knockdown USP8 significantly decreased tumor growth and USP8 overexpression enhanced tumor growth (Fig. 5I)."
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"Taken together, these results showed that inhibition of USP8 suppressed the tumor malignancies.Besides, we validated whether inhibiting USP8 could improve the sensitivity of HCCC9810 cells to pemigatinib."
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"Meanwhile, USP8 deficiency could reduce tumor invasion and migration and tumor size in an immunity-dependent manner, and improve anti-tumor immunogenicity."
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"Moreover, it was demonstrated in vivo that MnS x , on the one hand, mediated the activation of tumor autophagy by USP8 via intracellular H 2 S, while Mn 2+ promoted the maturation of dendritic cells, activated cytotoxic T lymphocytes and contributed to tumor eradication."
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"USP8 deficiency significantly reduces tumor migration and invasion and improves anti-tumor immunogenicity."
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"Our results indicated that knockdown of USP8 or administration of erastin significantly inhibited tumor growth in vivo, erastin treatment and USP8 depletion in combination significantly inhibited tumor growth in vivo than administration of erastin or USP8 depletion alone (Fig. 5L)."
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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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"These data together suggest that USP8 inhibition by its pharmacologic inhibitor or genetic deletion in combination with SAS treatment effectively suppresses tumor growth and enhances CD8 T cell infiltration in tumors."
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"Our results suggested that USP8 promotes tumor progression by regulating β-catenin."
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"USP8 inhibition in combination with PD-1/PD-L1 blockade increased CD8 T cell infiltration and diminished tumor growth, compared to immune checkpoint blockade monotherapy."
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"Inhibition of USP8 led to diminished tumor invasion, migration, and overall tumor size, enhancing anti-tumor immunity."
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"Compared with the control shRNA group, USP8 knockdown effectively reduced the size of tumors formed in a xenografted mouse model (Fig. 1K)."
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"Immunohistochemistry (IHC) analysis of the expression of prostaglandin-endoperoxide synthase-2 (PTGS2), a marker for the assessment of oxidative stress and ferroptosis in vivo, indicated the combination effect of knocking down USP8 and erastin treatment in triggering tumor ferroptosis in vivo (Fig. 1L)."
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"One 19-year-old female patient (patient 5) displayed Pattern 1 phenotype in a Crooke cell tumor driven by a known USP8 (exon 14) c.2152T>C, p. (Ser718Pro) somatic mutation found in additional analysis."
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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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"In vivo xenograft and metastasis experiments indicate that inhibition of USP8 suppresses tumor growth and lung metastasis."
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"Further analysis demonstrated that pharmacological inhibition or knockout of USP8 in HCC cells triggered ferroptosis and inhibited tumor growth both in vitro and in vivo."
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"It is also reported that CSCC tumor progression is highly promoted by USP8 by observing the significant correlation with the FIGO stage, parametrial invasion, stromal depth, lymph node metastasis, and[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"One of the main molecular alterations in USP8-driven tumors is an overactivation of the epidermal growth factor receptor (EGFR) signaling pathway, which induces ACTH production."
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"Moreover, USP8 depletion attenuated tumor growth upon TRAIL injection in a xenograft model using cervical cancer cells."
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"Heterozygous deletion of Usp8 impedes colon tumorigenesis and tumor progression in a murine colorectal cancer model."
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"USP8 also promotes tumor metastasis, invasion, and epithelial‐mesenchymal transition in response to TGF‐β/SMAD signaling."
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"Notably, USP8 inhibition in combination with ferroptosis inducers suppresses the tumor growth and promotes CD8 T cell infiltration in the tumor microenvironment, which sets up a situation that makes the PD-1/PD-L1 blockade more effective in vivo."
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"In vivo using xenograft and tail vein injection mouse models indicated that inhibition of USP8 significantly reduced tumor growth and inhibited lung metastasis."
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