IndraLab

Statements



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"The knockout of USP22 in pancreatic ductal adenocarcinoma cells results in reduced myeloid cells infiltration and increased tumor infiltration of NK cells and T cells, leading to a synergistic response with combined immunotherapy (59)."

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"Increased infiltration of NK cells within the TME is a favorable prognostic factor in several solid tumors [35]; however, USP22 has been reported to suppress NK cell infiltration by altering the transcriptome of pancreatic cancer (PC) cells [36]."

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"Inhibiting USP22 would lead to less activation of immune cells to immunosuppressive microenvironment or more infiltration of immune cells to immune-sensitive status, this issue of deeply associated mechanisms needs to consistently be solved."

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"USP22 in PC cells interacts with SAGA/STAGA to affect the immune microenvironment, and USP22 deficiency promotes T-cell and NK cell infiltration and inhibits tumor metastasis (116)."

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"We report that deletion of USP22 in pancreatic tumor cells reduced the infiltration of myeloid cells and promoted the infiltration of T cells and NK cells, leading to an improved response to combination immunotherapy."

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"The decreased expression of the deubiquitinase USP22 in pancreatic cancer cells promoted the infiltration of natural killer and T cells, thereby enhancing the anti-tumor immune response of the TME.91 Ubiquitination modification also regulates T cells to promote the differentiation of other cells."

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"In mouse models of hepatocellular carcinoma, knockout of Usp22 increases the infiltration of tumor-infiltrating lymphocytes, augments anti-tumor immunity, and synergizes with anti-PD-L1 treatments and chemotherapy (29)."

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"Tumor cell-derived CXCL1 and ubiquitin-specific protease 22 (USP22) were shown to decrease T cell infiltration and response to immunotherapy in PDAC."