IndraLab

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USP22 inhibits Neoplasms. 16 / 16
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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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"Moreover, genetic depletion of USP22 increased tumor immunogenicity and tumor-infiltrating lymphocytes."
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"Notably, although knocking down USP22 only mildly reduced tumor growth, it significantly increased the sensitivity of tumors to Taz."
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"In addition to its cancer cell-intrinsic roles, USP22 has been recently discovered to suppress tumor immunosurveillance through potentiating Foxp3 + regulatory functions as well as upregulating the expression of checkpoint receptors PD-L1 and CD73 ."
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"Usp22 promotes oncogenic c-Myc activation as well as indirectly antagonizes the tumor-suppressive function of p53, and clearly diminishes tumor growth in in vitro and in vivo LLC1 models (55)."
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"USP22 also inhibits tumor proliferation via contributing to the deubiquitination of PTEN (Ren et al., 2022)."
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"USP22 was found to positively regulate stable FOXP3 expression and reduce tumor volume when ablated in Tregs."
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"Moreover, in NSCIC (86), USP22 deletion can promote the therapeutic effect of PD-L1-targeted tumor immunotherapy."
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"17 About the possible relationship among BMI1, EZH2, and USP22, it has been reported that USP22 increases BMI1: in gastric cancer, USP22 inactivation decreases the neoplasm growth, while high levels of BMI1 accelerate the cell cycle via INK4a/ARF and AKT."
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"Interestingly, it was demonstrated that silencing USP22 inhibited proliferation in bladder cancer cells (Lv et al., 2011) leading to cell cycle arrest, inhibition of autophagy and decreased tumor progression representing a potential target for cancer therapy."
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"Apart from activating oncogenes such as BMI-1 and c-MYC , USP22 can inhibit the expression of tumor suppressors such as TP53 through ubiquitination , thus promoting proliferation of tumors [ 87 ] ."
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"52 , 53 , 54 On the other hand, in colorectal cancer, loss of USP22 can activate the mTOR/PI3K/Akt pathway, exacerbating the tumor progression caused by Apc mutations in colorectal cancer."
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"In addition to its cancer cell-intrinsic roles, USP22 has been recently discovered to suppress tumor immunosurveillance through potentiating Foxp3 regulatory functions32 42 as well as upregulating the expression of checkpoint receptors PD-L1 and CD73.43 44 Therefore, targeting USP22 presumably achieves both chemo- and immuno-therapeutic efficacy."
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"Based on these observations, the authors hypothesized that USP22 inhibition could simultaneously promote anti-tumor immunity and target tumors driven by USP22 upregulation and pathogenic H2Bub1 deplet[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"The deubiquitinating enzyme USP22 has been identified as a promoter of ACC and ACLY transcription by stabilizing PPARγ protein, resulting in a two- to three-fold increase in lipid content, a mechanism observed in 60% of HCC samples.73 Animal studies have shown that USP22 can reduce tumor volume by 70%, whereas PPARγ inhibitors can reverse lipid accumulation and tumor growth."
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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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