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发布于:2020-11-27 20:50:46  访问:0 次 回复:0 篇
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Quantification of M phase cell arrest induced by DCZ is shown on the right panel.However, the level of phosphorylated CHK was not affected.Based on the fact that DCZ was an anticancer agent that induced DNA sell Dantrolene sodium salt damage and the M phase cell cycle arrest, we speculated that DCZ might also activate the ATMATRCHK signaling pathway.Towards this, both NCIHR and RPMIR cells were treated with DCZ and subsequently exposed to KU, an ATM inhibitor.Our results showed that DCZ suppressed HR but had little effect on NHEJ. DNA damage and aberrant DNA repair usually turn cells into aneuploids, which may lead to mitotic catastrophe. Our results showed that following treatment with DCZ, both NCIHR and RPMIR cells exhibited multipolar mitotic spindles. The CI is considered the gold standard to define the synergism of drugdrug interactions. CI values always represents an additive effect, while CI values and indicate synergistic and antagonistic interactions, respectively.Thus, a low CI value stands for strong synergism and vice versa.According to our previous study, DCZ showed synergism with BTZ in MM.Furthermore, DCZ was synergistic with the histone deacetylase over a broad range of concentrations, and the synergy Targetmol‘s Dantrolene sodium salt increased with higher panobinostat doses.The body weight of the mice was monitored during the treatment to evaluate potential side effects, and day treatment with DCZ did not cause any changes in the animal weight. HE staining showed that cell shrinkage and fragmentation increased upon DCZ and combinational treatment. X, phosphoATM, and phosphoCHK were upregulated in vivo.Collectively, the data of the present study suggest that DCZ is a promising compound to counter BTZ resistance in MM in vivo and in vitro.DCZ inhibited cell proliferation in a dose and timedependent manner.Synergistic effect of DCZ and BTZ in MM cell lines.Western blot of GM phase related proteins in NCIHR and RPMIR cells treated with DCZ alone, BTZ alone and their combination for hto M DCZ.Both the G and M phase belong to the late stage of mitosis, and cells in these phases have the same DNA content.However, one of the most remarkable differences between the G and M phase is the chromatin condensation in the G phase and chromosome formation in the M phase.Next, we investigated the influence of DCZ on the expression of GM checkpoint proteins.The checkpoint pathways involved in DNA damage or errors are phylogenetically conserved according to the previous report.The function of active checkpoints is delaying cell cycle progression to facilitate DNA repair. During DNA damage, the key regulators in the checkpoint pathways, ATM and ATR kinases, are activated by phosphorylation that in turn phosphorylates HA.X via the checkpoint kinases CHK or CHK to induce cell cycle arrest. Thus, the G checkpoint is the last opportunity to halt the cycle and repair the DNA damage in cells that have escaped the G and S phase checkpoints.Based on this information, we investigated whether DCZ activated any of the upstream DNA damage signaling pathways.The comet assay and IF results showed that DCZ aggravated DNA fragmentation.HE staining of tumor sections for tumor histology after treatment.Therefore, the G checkpoint is the last opportunity to halt the cycle and repair DNA damage in cells that have escaped the G and S phase checkpoints.
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