IndraLab

Statements


USP22 activates NSCLC. 8 / 8
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"Our study has deepened the understanding of how USP22 promotes NSCLC tumorigenesis."

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"Taken together, our results suggest that USP22 promotes NSCLC tumorigenesis in vitro and in vivo through MDMX upregulation and subsequent p53 inhibition."

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"For instance, USP22, a ubiquitin hydrolase, enhances the proliferation, angiogenesis, and recurrence of NSCLC."

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"However, whether USP22 promotes tumorigenesis in NSCLC remains unclear."

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"In summary, our results suggest that USP22 promotes NSCLC tumorigenesis in vitro and in vivo through MDMX upregulation and subsequent p53 inhibition."

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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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"USP22 promotes the invasion of NSCLC in a TFAP2A-dependent manner [11]."

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"Therefore, our results from the mouse xenograft model demonstrate that USP22 silencing inhibits NSCLC tumorigenesis in vivo through regulating the MDMX-p53 pathway."