IndraLab

Statements



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"As shown by the CCK-8 assay, A549 and H1299 cell proliferation was promoted by the overexpression of USP5 but impaired by its knockdown (Figure 3D,3E)."

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"Our cell model data together with Xue’s data (35) have clarified that USP5 promotes the proliferation and metastatic malignant biological behaviors of NSCLC cells, thus providing a plausible explanation for the contribution of high level of USP5 to poor prognosis of NSCLC.As a member of the USP family, USP5 has been found to cleave both linear and branched ubiquitin polymers, and regulates protein ubiquitination, stability, and function (24,36)."

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"23, 24, 25 NSCLC studies have shown that high expression levels of USP5 and USP7 in lung cancer tissue promote lung cancer cell proliferation by stabilizing beta-catenin."

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"CCK-8 assay and colony formation experiments showed that overexpression of USP5 in Panc1 cells dramatically increased the proliferation."

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"These data indicated that USP5 promoted ovarian cancer cell proliferation and cell cycle progression through regulating HDAC2."

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"USP5 was recently found to stabilize c-Maf protein and promote myeloma cell proliferation and survival XREF_BIBR."

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"Overexpression of USP5 accelerates the proliferation of glioblastoma cells, which is abrogated by knockdown of FOXM1."

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"Deubiquitinase USP5 promotes non-small cell lung cancer cell proliferation by stabilizing cyclin D1."

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"Further functional investigation also showed that Usp5 knockdown suppressed cell proliferation, migration, drug resistance and induced apoptosis; on the other hand, Usp5 overexpression promoted colony formation, migration, drug resistance and tumorigenesis."

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"In HCC cells, USP5 knockdown inhibited cell proliferation, migration and drug resistance, while induced apoptosis and activated p14 -p53 signaling [16]."

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"USP5 is up-regulated in pancreatic cancer tissue and promotes cell viability and proliferation."

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"USP5 is overexpressed in colorectal cancer tissues and promotes colorectal cancer cell proliferation and resistance to chemotherapeutics."

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"Knockdown of USP5 has been found to inhibit proliferation of various cancer cell lines [37,193]."
| PMC

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"The above results showed that USP5 could promote NSCLC cell proliferation via upregulating the CCND1 protein level through deubiquitylation and stabilization of CCND1."

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"It has been reported that USP5 promotes tumor proliferation and tumorigenesis through the deubiquitination of histone deacetylase 2 (HDAC2) and beta-catenin."

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"The siRNA induced knockdown of Usp5 inhibited cell proliferation, migration ability and drug resistance."

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"Furthermore, the colony formation assays also showed that USP5 knockdown inhibited proliferation of PANC-1 and SW1990, two PDAC cell lines.To further evaluate the role of USP5 in PDAC progression, six[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"We concluded that USP5 promoted the proliferation of trophoblast cells via the up-regulation of the Wnt and beta-catenin signaling pathway."

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"Taken together, these results suggested that USP5 could evidently promote pancreatic cancer cells proliferation and metastasis."

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"The cells treated with USP5 OE and siHDAC2 showed the similar expression levels of HDAC2 and p27 as those treated with Vector and control siRNA (siNC), indicating that USP5 down-regulated p27 expression via regulating HDAC2.Further, CCK-8 (Figure 4G) and flow cytometry analyses (Figure 4H) showed that HDAC2 knockdown partially abrogated cell proliferation promoted by USP5 overexpression."

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"HDAC2 knockdown partially abrogated USP5-promoted ovarian cancer cell proliferation."

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"Our previous studies demonstrated that the deubiquitinase USP5 stabilizes c-Maf and promotes myeloma cell proliferation and survival; therefore, the USP5 and c-Maf axis could be a potential target for myeloma therapy."

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"By decreasing CCND1 ubiquitination, USP5 stabilizes and upregulates its protein level and consequently promotes NSCLC proliferation."

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"USP5 overexpression enhanced, whereas USP5 silencing impaired the cell proliferation and colony formation of NSCLC cells in vitro."

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"Inhibition of USP5 activity suppresses NSCLC cell proliferation in vitro and tumor growth in vivo."

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"Disruption of USP5 profoundly repressed cell proliferation by inducing cell cycle G0/G1 phase arrest in ovarian cancer cells."