IndraLab

Statements

USP18 activates Neoplasm Invasiveness. 9 / 9
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"Furthermore, silencing USP18 attenuated HNSC cell proliferation, invasion, and migration, while overexpression of USP18 exerted converse effects."
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"Subsequently, we validated that USP18 modulated PLK1 to activate the mTORC1 pathway, thereby facilitating HNSC cell proliferation, invasion, and migration."
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"Moreover, recent studies have shown that deletion of USP18 reduces tumor cell proliferation, migration, and invasion [93]."
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"In functional experiments , USP18 knockdown significantly inhibited ESCC invasion and metastasis in vitro ."
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"Silencing USP18 suppressed COAD cell proliferation and invasion via destabilizing extracellular signal-regulated kinase (ERK) protein and suppressing ERK downstream pathways."
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"Furthermore, our results shown that knockdown of USP18 suppressed the migration and invasion abilities of ESCC cells by promoting the process of epithelial-mesenchymal transition (EMT)."
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"Migration and invasion assays indicated that USP18 silencing obviously inhibited the mobility and invasiveness of ESCC cells ( Fig. 2 C and D)."
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"These data clearly suggested that USP18 promotes the invasion and metastasis of ESCC cells in vitro and in vivo , indicating that USP18 might function as an oncogene for ESCC.As is known, the EMT proc[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"In this cancer, USP18 enhances the protein stability of zinc finger E-box-binding homeobox 1 (ZEB1) through the decreased ubiquitination of ZEB1, increasing the migration and invasion abilities of ESCC cells [90]."
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