IndraLab

Statements

USP47 activates Cell Survival. 11 / 14
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"In the present study, USP47 was identified as a target of miR-454, and USP47 knockdown significantly inhibited cell viability and DDP resistance in NPC cells compared with the shNC group."
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"It was recently demonstrated that silencing of USP47 inhibits cell survival and sensitizes cells to DNA damaging agents (Peschiaroli et al., 2010)."
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"USP47 has also been described as an interaction partner for the ubiquitin E3 ligase complex, beta-TrCP, with the authors of this study showing that silencing of USP47 expression inhibits cell survival and sensitises cells to chemotherapeutic agent induced apoptosis [XREF_BIBR]."
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"Additionally, the utilization of AZD6738 (50nM), an ATR pathway inhibitor, partially inhibits USP47 knockdown induced suppression of cell viability in CML cells."
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"The CCK-8 assay results demonstrated that USP47 knockdown significantly reduced cell viability compared with the shNC group , which was significantly reversed by co-transfection with miR-454 knockdown in 5-8F / DDP and SUNE-1 / DDP cells ( Fig. 6C ) ."
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"Silencing of USP47 inhibits cell survival and sensitizes cells to chemotherapic agent induced apoptosis."
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"Compared with the shNC group, USP47 knockdown significantly suppressed NPC cell viability and DDP resistance, which was significantly reversed by co-transfection with miR-454 inhibitor."
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"Silencing of USP47 decreases cell survival and augments the cytotoxic effects of antitumor drugs on a variety of tumor cells, including osteosarcoma and breast cancer cell lines."
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"Compared with the shNC group , USP47 knockdown significantly suppressed NPC cell viability and DDP resistance , which was significantly reversed by co-transfection with miR-454 inhibitor ."
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"The CCK-8 assay results demonstrated that USP47 knockdown significantly reduced cell viability compared with the shNC group, which was significantly reversed by co-transfection with miR-454 knockdown in 5-8F/DDP and SUNE-1 and DDP cells (XREF_FIG)."
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"We found that USP47 contributes to cell viability and chemoresistance in NCI-N87 gastric carcinoma cells treated with etoposide and camptothecin."
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