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https://www.selleckchem.com/products/dnqx.html There has been accumulating evidence suggesting nitric oxide donors as such targeting agents and considering their pleiotropic antitumor activities, including both the reversal of chemo and immuno-resistance of various unresponsive resistant cancers. The in vitro and in vivo preclinical findings corroborate the sensitizing antitumor activities of nitric oxide donors. In addition, a few clinical findings with NO donors that have been applied in patients have corroborated their antitumor and sensitizing activities in combination with standard therapies. In this review, the role and underlying mechanisms by which nitric oxide donors sensitize cancer resistant cells to both chemotherapy and immunotherapy are briefly described. Transcriptional coactivators p300 and CBP catalyze the acetylation of lysine residues in histone proteins. Upregulation of p300 and CBP has been associated with lung, colorectal and hepatocellular cancer, indicating an important role of p300 and CBP in tumorigenesis. Recently, the novel p300 and CBP-selective inhibitor A485 became available, which was shown to inhibit proliferation of 124 different cancer cell lines. Here, we found that downregulation of EP300 or CREBBP enhances apoptosis upon TRAIL stimulation in non-small-cell lung cancer (NSCLC) cells. A485 upregulates pro- and anti- apoptotic genes at the mRNA level, implying an apoptosis-modulating effect in NSCLC cells. However, A485 alone does not induce apoptosis. Interestingly, we observed that the number of apoptotic cells increases upon combined treatment with A485 and TRAIL. Therefore, A485, as a TRAIL-sensitizer, was used in combination with TRAIL in wild type of NSCLC cell lines (HCC827and H1650) and cells with acquired erlotinib resistance (HCC827-ER and H1650-ER). Our results show that the combination of A485 and TRAIL synergistically increases cell death and inhibits long-term cell proliferation. Furthermore, this combination inhibits

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