IndraLab

Statements

USP7 activates Carcinogenesis. 19 / 19
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"Role of the USP7/FOXO3A axis in environmentally relevant doses of arsenic-induced lung carcinogenesis: Insights from bioinformatics analysis and model of human epithelial cell malignant transformation."
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"Increased USP7 expression has been demonstrated in numerous tumor entities and overexpression of USP7 was shown to promote carcinogenesis and to impair successful therapy [19,20,21,22]."
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"Also , USP7 regulates PTEN localization and eventually inducing tumorigenesis ."
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"USP7 also promotes carcinogenesis through aberrant activation of the Wnt signalling pathway and stabilization of HIF-1alpha ."
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"These clinical and functional studies suggest that aberrant activation or overexpression of HAUSP may promote tumorigenesis, making HAUSP a target for therapeutic intervention in strategies to restore normal PTEN localization and tumor-suppressive function, as we discuss further below."
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"Inhibition of USP7 significantly counters resistance to Dox and paclitaxel in TNBC cells, thus diminishing tumorigenesis and distant metastasis in an orthotopic BC mouse model [93]."
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"YY1 and USP7 promoted tumorigenesis and metastasis of colorectal carcinoma in vitro and in vivo."
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"Another study further revealed that LINC00265 was able to regulate ZMIZ2 and USP7-mediated stabilization of β-Catenin, thereby facilitating colorectal tumorigenesis [39]."
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"USP7 also promotes carcinogenesis through aberrant activation of the Wnt signalling pathway and stabilization of HIF-1alpha."
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"30 , 31 , 32 Furthermore, USP7 contributes to carcinogenesis by inappropriately activating the Wnt signalling pathway 33 , 34 and stabilising HIF‐1α."
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"In addition, we also verified from the DepMap, HPA, and UCSC Xena databases that Usp7 is a driver of NSCLC oncogenesis."
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"Therefore, USP7 is able to promote breast carcinogenesis through the USP7/PHF8/cyclin A2 axis (Wang et al., 2016b; Xia et al., 2019)."
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"In addition, USP7 was found to stabilize LSD1, further inhibit the p53 signaling pathway, and promote tumorigenesis and metastasis of glioblastoma [34]."
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"Stabilization of G3BP2 by PRMT5 and USP7 promotes tumorigenesis of carcinoma cells."
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"USP7 (HAUSP), a well-known regulator of p53 and MDM2 availability, deubiquitylates HIF-1α under normoxia and promotes carcinogenesis [58] ( Table 1 )."
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"Aberrant activation or overexpression of USP-7 might promote oncogenesis, making this protein a promising target for cancer treatment [29]."
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"USP7 ( HAUSP ) , which is known to regulate p53 availability in the cell through its direct stabilization and / or indirectly by stabilizing MDM2 [ 118 ] , was shown to have the ability to deubiquitylate HIF-1alpha under normoxia and to promote epithelial-mesenchymal transition and carcinogenesis [ 119 ] ."
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"Due to the ubiquitous expression of USP7, its association with viral infection, and the observation that aberrant activation or overexpression of USP7 may promote oncogenesis, USP7 has become an attractive therapeutic target and a number of small-molecule inhibitors have been described."
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"MDM2 and p53 genes are among the most important oncogenes in terms of their relevance to USP7-induced carcinogenesis."
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