IndraLab

Statements


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"Studies of USP4 knockout mice revealed that USP4 upregulates tumor growth in an mTORC1-dependent manner."

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"In contrast, depletion of USP4 significantly inhibited proliferation, migration, and invasion abilities in vitro and suppressed tumor growth and metastasis in vivo."

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"USP4 induces ESCC cell proliferation and tumor growth."

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"Meanwhile , knockdown of USP4 led to reduced tumor size , as well as reduced expression level of p-S6 , which could be rescued by the expression of Rheb-K8R ( Fig. 7d-f ; Supplementary information , Fig. S7b ) ."

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"Knockdown of USP4 significantly inhibited tumor growth in C57BL/6 mice ( Fig. 6 A–C)."

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"Together, these findings indicate that USP4 promotes cell proliferation and tumor growth in ESCC."

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"Furthermore, IRF3 knockdown rescued the reduced tumor growth caused by USP4 inhibition ( Fig. 6 I–K), and also decreased total T cells and CD8 + T cells infiltration while increased Tregs infiltration[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"USP4 modulates tumor growth factor TGF-β signaling to regulate immunosuppressive pathways in the tumor microenvironment."

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"In vivo, treatment with U0126 further enhanced the suppression of tumor growth induced by downregulation of USP4 (Fig. 7D–F)."

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"In our study, we indicated that the tumor-promoting role of USP4 in PC relied on interacting with TRAF6 and the activation of NF-κB signaling pathway."

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"The results of tumorigenesis experiment in nude mice showed that USP4 could promote tumor proliferation and promote tumor in vivo.In summary, we found that USP4 is highly expressed in lung adenocarcinoma."

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"Bioinformatics tools were used to explore the potential mechanisms of the tumor-promoting role of USP4 in PC."

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"With the corresponding treatment, USP4 knockdown with anti -PD-L1 antibody treatment significantly reduced tumor growth compared to monotherapy with anti -PD-L1 antibody ( Fig. 7 A–C)."