ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR189/002/SRR18961102/SRR18961102.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR189/012/SRR18919212/SRR18919212.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR189/084/SRR18904384/SRR18904384.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR189/010/SRR18919210/SRR18919210.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR189/082/SRR18904382/SRR18904382.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR189/004/SRR18961104/SRR18961104.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR189/013/SRR18919213/SRR18919213.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR189/011/SRR18919211/SRR18919211.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR189/085/SRR18904385/SRR18904385.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR189/001/SRR18961101/SRR18961101.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR189/003/SRR18961103/SRR18961103.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR189/083/SRR18904383/SRR18904383.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR189/014/SRR18919214/SRR18919214.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR189/005/SRR18961105/SRR18961105.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR189/081/SRR18904381/SRR18904381.fastq.gzprimaryOK200GenomicsMaria Sklodowska-Curie National Research Institute of Oncology, Gliwice Branchhttps://www.ebi.ac.uk/ena/browser/view/PRJNA831359Actinomycin D, nutlin-3a and camptothecin are activators of the p53 tumor suppressor protein. These substances induce different posttranslational modifications of p53 and consequently they activate p53 to different degrees. Nutlin-3a appears to be the weakest activator, whereas camptothecin - the strongest. Interestingly, actinomycin D and nutlin-3a, when applied together (A+N), synergize in activation of p53 and consequently, in transcriptional regulation of its target genes. The goal of the project was to find out genes up- or down-regulated by treatment of cells with either actinomycin D, nutlin-3a, A+N or camptothecin in order to identify the new candidate, p53-regulated genes.xref:EuropePMC:PMC11416401xref:EuropePMC:PMC11274236ENAActinomycin, human being, Transcriptome Profile, ActD, Neoplasms, Benign Neoplasm, Gene Expression Profile, Gene, 13)oxatetra-azacyclohexadecin-10-yl)-4, Profiles, Tumor, Malignant, 10, Human, 11, (+)-camptothecin, Homo sapiens, 4, 5, Cosmegen Lyovac, 7, Man, 21, treatment, 1-i)(1, 13-bis(1-methylethyl)-1, Man (Taxonomy), Malignancy, Profile, 4-ethyl-4-hydroxy-, 9-dicarboxamide, man, Signatures, Actinomycin D, Neoplasias, D-camptothecin, Expression Signature, malignant neoplasm, Lyovac Cosmegen, disease management, Transcriptomes, Therapies, 14(4H, Malignancies, 9-trimethyl-6, Camptothecine, 2-b)quinoline-3, Cancer, Tumors, 7)indolizino(1, Therapy, CPT, Transcriptome, Malignant Neoplasm, Modern, Expression Profiles, LyovacCosmegen, 22-Secocamptothecin-21-oic acid lactone, (S)-, (+)-camptothecine., Cell, Cosmegen, actinomycin IV, whole transcriptome, Gene Expression, MT, Benign, Expression Signatures, Gene Expression Signatures, Neoplasm, Gene Expression Signature, N'-bis(hexadecahydro-2, 14-pentaoxo-1H-pyrrolo(2, 1H-Pyrano(3', Expression Profile, actinomycin C1, Transcriptome Profiles, primary cancer, Lyovac-Cosmegen, 2-amino-N, (S)-(+)-camptothecin, Benign Neoplasms, 6-dimethyl-3-oxo-3H-phenoxazine-1, Cancers, Treatments, malignant tumor, human, Malignant Neoplasms, 20(S)-camptothecine, Therapeutic, Gene Expression Profiles, 12H)-dione, Dactinomycin, Modern Man, Treatment, Meractinomycin, Signature, 4':6, Lyovac, NeoplasiafalseTranscriptome changes following treatment of human cancer cells with actinomycin D, nutlin-3a or camptothecin2023-05-192022-04-26PRJNA831359