IndraLab

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USP22 activates HYCC1. 16 / 16
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"These results suggest that the expression of USP22 may promote VM formation in HCC-derived cell lines.Next, we turn to determine the effect of USP22 on migratory and invasive behaviors of HCC cells, transwell assays were performed in shUSP22 Huh7 or shUSP22 PLC/PRF/5 cells."
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"Taken together, our results indicate that USP22 promotes HCC cell growth and VM formation in mice.Having revealed that USP22 maintains ZEB1 stability, we next examined the expression of USP22 and ZEB1 in 24 pairs of human HCC pathological sections by immunohistochemistry."
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"Our results revealed that USP22 promoted tumorigenesis and progression via an FKBP12/mTORC1/autophagy positive feedback loop in HCC."
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"Therefore, USP22 activates the mTORC1 signaling pathway both in vitro and in vivo.2.3 USP22 promotes tumorigenic potential and sensitizes HCC toward rapamycin in vitro and in vivo."
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"2.1 Overexpression of Usp22 accelerates c-Myc/NRasGV12-induced HCC in mice."
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"Under the treatment of Lenvatinib, USP22 knockdown inhibited the cell viability of drug-resistant HCC cells and promoted the apoptosis of drug-resistant cells."
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"Simply put, USP22 may activate the SIRT1–AKT–MRP1 pathway and consequently promote MDR in human HCC cells (226)."
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"Our data demonstrate that USP22 deletion inhibits the migration and invasion of HCC cells (Fig. 5F, G and Supplementary Fig. S6D)."
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"Ablation of USP22 in immunosuppressive regulatory T cells leads to reduced tumor burden in several cancers.56 Importantly, USP22 promotes tumorigenesis and progression in HCC, by promoting stemness.53,57As hepatic expression of CXCL13 and SCF genes strongly correlated with tumor burden, we tested their potential as circulating HCC biomarkers."
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"USP22 promotes HCC-derived cell growth/invasion/Vascular Mimicry (VM) formation and angiogenesis."
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"The USP22 increases growth and metastasis of HCC cells via inducing Wnt/β-catenin signaling."
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"In the current study, we demonstrated that the ubiquitin hydrolase USP22 contributed to HCC tumorigenesis and promoted tumorigenic potential of HCC, suggesting an oncogenic role of USP22 consistent with the majority of published studies."
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"An illustrative example is the positive feedback loop between USP22 and HIF1α, which promotes glycolysis and stemness in HCC following TP53 mutation [94]."
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"In HCC, it has been reported that USP22 modulates HCC tumorigenesis via modulating PPARγ protein ( Ning et al., 2022 )."
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"Furthermore, we provided the evidence to show that knockdown of USP22 inhibited HCC growth in tumor-bearing nude mice."
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"The results showed that, overexpression of USP22 significantly promoted the growth of HCC, and knockdown of ZEB1 inhibited the effect of USP22 on tumor growth (Fig. 6G–J), suggesting that ZEB1 was involved in the development of HCC, and the promotion of HCC growth by USP22 was partially related to ZEB1.In addition, the results from immunohistochemistry showed that USP22 depletion decreased USP22, ZEB1, or VEGFA expression in xenograft tumors."
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