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USP22 activates Carcinogenesis. 24 / 24
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"Together, these results support that USP22 promotes CRC cell proliferation and tumorigenesis by stabilizing FASN."
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"Together, these results suggest that FASN is stabilized by USP22 in colorectal cancer, and the dysregulated USP22/FASN axis is a important driver for tumorigenesis."
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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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"Further , USP22 is shown to facilitate cell-cycle progression and colorectal tumorigenesis by targeting CCNB1 while in glioblastoma , USP22 promotes tumorigenesis via stabilizing KDM1A [ 89,90 ] ."
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"Genetic and pharmacological inhibition of PPARγ abolished the regulatory effect on ACC and ACLY transcription, and significantly decreased lipogenesis and tumorigenesis caused by USP22 expression both in HCC cells and xenograft tissues."
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"Silencing of USP22 enhanced T cell cytotoxicity and blocked lung tumorigenesis."
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"In addition , we find that USP22 promotes de novo fatty acid synthesis and contributes to HCC tumorigenesis , however , this tumorigenicity is suppressed by inhibiting the expression of PPARgamma , ACLY , or ACC in in vivo tumorigenesis experiments ."
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"In our study, we found that knockdown of DUSP1 enhanced the AKT signaling pathway, whereas repression of DUSP1 by E2F6 was required for USP22-mediated carcinogenesis."
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"We wanted to elucidate the mechanisms by which miR-30e-5p inhibits USP22-mediated tumorigenesis in NSCLC.Previous studies have demonstrated a role for miR-30e-5p in downregulating oncogenic pathways, [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"The deubiquitylase USP22 is frequently overexpressed in cancer and contributes to tumorigenesis by driving cell cycle progression."
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"Our study has deepened the understanding of how USP22 promotes NSCLC tumorigenesis."
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"In addition, we find that USP22 promotes de novo fatty acid synthesis and contributes to HCC tumorigenesis, however, this tumorigenicity is suppressed by inhibiting the expression of PPARγ, ACLY, or ACC in in vivo tumorigenesis experiments."
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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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"Thus, miR-485-5p/USP22 axis was critically involved in linc00265-induced oncogenesis."
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"Evidently , HnRNPA1 is a downstream transcription regulator of c-Myc ( proto-oncogene ) whereas USP22 positively regulates c-Myc stability and promotes tumorigenesis [ 35,36 ] ."
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"The mechanism by which USP22 promotes NSCLC tumorigenesis is that USP22 can directly bind and upregulate MDMX (E3 ubiquitin ligase) in NSCLC cells and subsequently inhibit the P53 pathway to promote NSCLC tumorigenesis (76) ( Table 1 )."
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"The results showed that overexpression of Usp22 accelerated tumorigenesis, whereas Usp22 ablation decelerated it in the mouse HCC model (Figure 1D,E)."
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"These results indicate that AKT-mediated phosphorylation is critical for USP22 stabilization during EPI-induced tumorigenesis."
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"In the future, the discovery of data-driven markers will become a trend, and multiparameter and composite biomarker prognostic prediction models constructed based on high-throughput sequencing data ma[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"As a result, we found that tissue-specific Usp22 overexpression accelerated tumorigenesis, whereas Usp22 ablation decelerated it in a c-Myc/NRasGV12-induced HCC mouse model and that the mammalian target of rapamycin complex 1 (mTORC1) pathway was activated downstream."
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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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"USP22 promotes non-small cell lung cancer and retinoblastoma tumorigenesis via p53 inhibition [74,75] ."
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"In support of this, gain-of-function or loss-of-function studies revealed that USP22 stimulates lipogenesis from glucose in cultured hepatocytes and subsequently contributes to tumorigenesis [193]."
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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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