WebHepatocellular carcinoma (HCC) is the most common primary liver neoplasm and current systemic chemotherapy are mostly ineffective. Paclitaxel (PTX) has a clinically significant effect on many malignant tumors. Cells treated with PTX undergo reversible mitotic arrest and although high doses can cause side effects it may also induce apoptosis.
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WebMay 19, 2016 · Microtubule poisons inhibit spindle function, leading to activation of spindle assembly checkpoint (SAC) and mitotic arrest. Cell death occurring in prolonged mitosis is the first target of microtubule poisons in cancer therapies. However, even in the presence of microtubule poisons, SAC and mitotic arrest are not permanent, and the surviving cells … WebAbstract. Purpose: To study the kinetics of gene expression alterations following radiation exposure of isogenic HCT116 p53 +/+ and HCT116 p53-/- cell lines. Materials and …
Web(a) Most HCT116 cells escape from mitosis at 24 h after paclitaxel treatment. (b) In contrast, almost 40% of HT29 cells are still in mitosis after 48 h of paclitaxel treatment. The mitotic... WebAnother outcome is mitotic slippage, in which cells exit mitotic arrest, enter pseudo-G 1 phase without cytokinesis, and then become tetra-ploid. These cells can then either die quickly or die in a ... The colorectal cancer cell line HCT116, a mitotic checkpoint-proficient near-diploid cell line, was used in this study. This cell line is ...
WebMay 19, 2016 · To determine whether SIRT2 is involved in SAC functions, we used the colorectal cancer cell line HCT116 (a mitotic checkpoint-proficient near-diploid cell line), … WebJan 1, 2024 · Depression of mitotic cell death in HCT116 (p53+/+) cells with SIRT2 suppression was released by suppression of P/CAF or p21. Thus, the P/CAF-MDM2-p53-p21 axis enables the escape from mitotic cell death and confers resistance to nocodazole in HCT116 (p53+/+) cells with SIRT2 suppression.
WebWe previously profiled the anti-mitotic drug response of 11 mammalian cell lines, including cancer cell lines derived from the lung (A549, H460), colon (HCT116, HT29), breast (MCF7, MDAMB435S), ovary (OVCAR5), cervix (HeLa), prostate (PC3), and bone (U-2 OS) as well as a normal cell line, RPE.5
WebNational Center for Biotechnology Information ez grass scottsWebSince it has been demonstrated that cell senescence can be induced by mitotic slippage [30, 31], we evaluated, in HCT116 Rel cells, the presence of tetraploid/polyploid cells, which are... ez gridWebNov 1, 2024 · To study the fate of cells postslippage, we chose mitotic slippage–prone cells, namely osteosarcoma U2OS cells, colorectal carcinoma HCT116 cells, and … ez grgWebMar 1, 2024 · Mitotic slippage was also observed with even higher frequency in JH-Eso-Ad1 cells (28.6%; n = 7) ... (HCT116), colorectal adenocarcinoma (HT29), osteosarcoma (U2OS) and cervix adenocarcinoma (HeLa) cells [34, 35]. These findings led to speculate that increased accumulation of Ndc80, as part of the Ndc80 complex, might influence the … ez grass seedWebApr 30, 2009 · C, detection of phosphorylated Aurora-A and Aurora-B kinases on Western blots using lysates from mitotic HCT116 cells treated with nocodazole for 14 h followed by incubation with MG132 in the presence or absence of 2 μmol/L Gö6976 or 2 μmol ... Mitotic checkpoint slippage in humans occurs via cyclin B destruction in the presence of an … hidrica maringaWebDownload scientific diagram Influence of PHA680632 on cell cycle in p53wt vs p53−/− HCT116 cells. (A and B) analysis of the cell cycle. (A) Quantitative data of cell cycle distribution after ... ez green fertilizerWebUSP49 is required for the spindle checkpoint and its depletion causes mitotic slippage upon nocodazole treatment. A, B shUSP49.77, shUSP49.79 or pLKO.1 (control) vectors were transfected into... ezgrid