15357163mct141093t-sup-143010_0_supp_2806300_nhkd1c.xlsx (63.29 kB)
Supplementary Table 3 from ATF4 Gene Network Mediates Cellular Response to the Anticancer PAD Inhibitor YW3-56 in Triple-Negative Breast Cancer Cells
datasetposted on 2023-04-03, 14:12 authored by Shu Wang, Xiangyun Amy Chen, Jing Hu, Jian-kang Jiang, Yunfei Li, Ka Yim Chan-Salis, Ying Gu, Gong Chen, Craig Thomas, B. Franklin Pugh, Yanming Wang
ATF4 associated genes
ARTICLE ABSTRACTWe 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.
Breast CancerCarcinogenesisSignal transductionCell CycleSignal transduction pathwaysCell Death And SenescenceTranscriptional control of apoptosisCell SignalingProtein serine-threonine kinasesComputational MethodsGene expression profilingEpigeneticsGene RegulationMechanisms of transcriptionPreclinical ModelsAnimal models of cancer