
IndraLab
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USP7 inhibits cell population proliferation. 57 / 57
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57
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"Combinatory inhibition of EZH2 and USP7 synergistically induces proliferation defect at relatively low concentrations (0.08 μM), which suggests a new therapeutic approach by co-targeting EZH2 and USP7 for DLBCL patients.Ubiquitously expressed genes USP7 and STAT3 were emergently marked by H3K27me3."
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"USP7 promotes the growth of non-small cell lung cancer cells by stabilizing Ki-67 protein, while metformin can inhibit the proliferation of esophageal cancer by upregulating USP7, suggesting that USP7 plays different roles in different types of tumors [50-52], USP4 and USP15 can stabilize TGF-β receptors and increase TGF-β-mediated EMT, leading to metastasis of hepatocellular carcinoma and glioblastoma [53-55]."
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"However, to the best of our knowledge, no studies have evaluated the mechanism and function of Usp7 in determining FGSC self-renewal and differentiation.In this paper, we report for the first time that Usp7 inhibited the proliferation of FGSCs and promoted their differentiation via genomic methylation."
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"In vitro studies also showed that downregulation of USP7 reduced proliferation of MHCC97-H cell lines and upregulation increased proliferation of Huh7 and Hep3B cell lines, suggesting that USP7 promoted HCC progression.31 Wang et al.70 performed wound healing assay and cell invasion assay to show that overexpression of USP7 can enhance invasion of HCC cells, while USP7-knockdown can suppress HCC invasion."
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"Overexpression of USP7 can regulate ERK1/2 signaling pathway, increase P53 expression, and inhibit G2/M transformation and proliferation of LUAD cells by deubiquitinating the M1, K6, K11, K27, K33, and K48 polyubiquitin chains of Raf-1 to reduce the level of RAF1 phosphorylation (7)."
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"42 It has also been shown that both up or down-regulation of USP7 protein expression reduces cell proliferation in colon cancer and tumour development in vivo, as a consequence of increasing p53 levels.43Interleukin-6 (IL-6) stimulates STAT3 activation in normal physiological conditions and is controlled via negative feedback mechanisms."