IndraLab

Statements

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"Ubiquitin specific peptidase 47 promotes proliferation of lung squamous cell carcinoma."
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"USP47 functions as a DUB for YAP in colorectal cancer, USP47 elevation leads to the stabilization of YAP and promotes colorectal cancer cell proliferation [11]."
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"Functional analysis shows that USP47 knockdown represses proliferation of CML cells sensitive or resistant to imatinib in vitro and in vivo."
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"Specifically, we demonstrate that USP47 is highly expressed in primary CML cells and promotes cell proliferation, while Usp47 knockout significantly prolongs the survival of BCR-ABL and BCR-ABL T315I -induced CML mice by reducing leukemia stem and progenitor cells."
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"USP47 knockdown inhibits proliferation of CML cells."
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"Knockdown of USP47 expression in PTC cell lines (TPC-1 and K1), decreased the cell proliferation mobility and invasion capacities, whereas USP47 overexpression in these cell lines showed an inverse effect and promoted cell glycolysis and glutamine metabolism."
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"Silencing Usp47 inhibits BCR-ABL T315I -induced CML and proliferation of KBM T315I in a xenograft mouse model."
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"USP47 deficiency impairs transcriptional activity of SATB1 target genes and inhibits proliferation, migration, and tumorigenesis (68, 69)."
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"We further show that USP47 deficiency represses cell proliferation and migration through SATB1."
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"USP47 functions as a DUB for YAP in colorectal cancer, USP47 elevation leads to stabilization of YAP and promotes colorectal cancer cell proliferation XREF_BIBR."
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"Therefore, we hypothesized that USP47 might contribute to liver regeneration by regulating proliferation of hepatocytes."
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"USP47 promotes colon cancer cell proliferation, tumorigenesis, and invasion partially through SATB1."
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"Yu et al also reported that USP47 and SMURF2 can mediate CC cell proliferation and tumor progression by reversibly manipulating SATB1 ubiquitination."
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"Conversely, USP47 or/and SATB1 overexpression ( Fig. S2F ) induces HCT116 cell proliferation ( Fig. 3 B)."
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"Taken together, our results reveal an oncogenic function of USP47 in promoting GC cell proliferation and metastasis, both in vitro and in vivo."
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"Consistent with previous reports, we observed that depletion of USP47 reduced cell proliferation only in the p53-positive A549 cell line and not in H1299 cells, which lack p53 expression."
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"Our results, which showed that the depletion of both USP7 and USP47 could more potently inhibit cell proliferation relative to the individual depletion of either alone, also support."
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"For example, USP47 overexpression accelerated ovarian cancer cell development, whereas USP47 knockdown inhibited gastric cancer cell proliferation."
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"Finally , we show that depletion of USP47 induces p53 and therefore inhibits cell proliferation , colony formation , and tumor progression in cancer cell lines and a mouse xenograft model ."
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"Besides, numerous results demonstrated that knockdown of USP47 increased the percentage of apoptosis and inhibited cell proliferation, which were consistence with our study."
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"Our findings indicated that USP47 deletion decreased cell proliferation and migration, whereas introducing SATB1 expression rescued cell growth and invasion.Ubiquitinases play major roles in several c[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Finally , we provide evidence that USP47 has oncogenic potential , and depletion of USP47 induces p53 by regulation of RPS2 and , therefore , inhibits cell proliferation , colony formation , and tumor progression in cancer cell lines and a mouse xenograft model in a p53-dependent manner ."
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"There were growing evidences supporting that USP47 promotes tumorigenesis, malignancies cell proliferation, drug resistance and epithelial-mesenchymal transition ( Hou et al., 2021 ; Park et al., 2022[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Additionally, USP47 promotes AML cell proliferation, enhances resistance to imatinib, and eliminates leukemia progenitor cells in CML by stabilizing Y-box-binding protein 1 (YBX1), a vital regulator of cell survival observed in multiple solid tumors and CML [39]."
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"Thus, knockdown of deubiquitylating enzyme USP47 decreases tumour cell proliferation, as well as increases the cytotoxic activity of chemotherapeutic agents ( Peschiaroli et al., 2010 )."
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"Functional experimental results showed that USP47 promoted the cell proliferation in vitro and tumor growth in vivo ."
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"USP47 reduction suppressed cell proliferation and colony formation of HCT116 cells, indicating USP47 involved in pathogenesis of CRC ( Fig. 1 D–E)."
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