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- W2002040608 abstract "Abstract We previously reported that a pan-PAD inhibitor, YW3-56, activates p53 target genes to inhibit cancer growth. However, the p53-independent anticancer activity and molecular mechanisms of YW3-56 remain largely elusive. Here, gene expression analyses found that ATF4 target genes involved in endoplasmic reticulum (ER) stress response were activated by YW3-56. Depletion of ATF4 greatly attenuated YW3-56–mediated activation of the mTORC1 regulatory genes SESN2 and DDIT4. Using the ChIP-exo method, high-resolution genomic binding sites of ATF4 and CEBPB responsive to YW3-56 treatment were generated. In human breast cancer cells, YW3-56–mediated cell death features mitochondria depletion and autophagy perturbation. Moreover, YW3-56 treatment effectively inhibits the growth of triple-negative breast cancer xenograft tumors in nude mice. Taken together, we unveiled the anticancer mechanisms and therapeutic potentials of the pan-PAD inhibitor YW3-56. Mol Cancer Ther; 14(4); 877–88. ©2015 AACR." @default.
- W2002040608 created "2016-06-24" @default.
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- W2002040608 date "2015-04-01" @default.
- W2002040608 modified "2023-10-17" @default.
- W2002040608 title "ATF4 Gene Network Mediates Cellular Response to the Anticancer PAD Inhibitor YW3-56 in Triple-Negative Breast Cancer Cells" @default.
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- W2002040608 doi "https://doi.org/10.1158/1535-7163.mct-14-1093-t" @default.
- W2002040608 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4394025" @default.
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