ArticleThe Biochemical journal2003
Daunorubicin-induced variations in gene transcription: commitment to proliferation arrest, senescence and apoptosis.
Article in The Biochemical journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 52 citations in OpenAlex.
- HIV-Tat upregulates the expression of senescence biomarkers in CD4Frontiers in immunology · 2025Article
- Pharmacological p38 MAPK inhibitor SB203580 enhances AML stem cell line KG1a chemosensitivity to daunorubicin by promoting late apoptosis, cell growth arrest in S-phase, and miR-328-3p upregulation.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024Article
- Targeting senescence as an anticancer therapy.Molecular oncology · 2022Review
- Senescence-Associated Secretory Phenotype as a Hinge Between Cardiovascular Diseases and Cancer.Frontiers in cardiovascular medicine · 2021Review
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- Convergence of therapy-induced senescence (TIS) and EMT in multistep carcinogenesis: current opinions and emerging perspectives.Cell death discovery · 2020Review
- Ascorbic Acid Chemosensitizes Colorectal Cancer Cells and Synergistically Inhibits Tumor Growth.Frontiers in physiology · 2018Article
- Small molecule compounds that induce cellular senescence.Aging cell · 2016Review
- Comparison of in vitro antileukemic activity of obatoclax and ABT-737.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- ALKBH3, a human AlkB homologue, contributes to cell survival in human non-small-cell lung cancer.British journal of cancer · 2011Article
- Novel derivative of benzofuran induces cell death mostly by G2/M cell cycle arrest through p53-dependent pathway but partially by inhibition of NF-kappaB.The Journal of biological chemistry · 2010Article
- Evaluation of molecular descriptors for antitumor drugs with respect to noncovalent binding to DNA and antiproliferative activity.BMC pharmacology · 2009Article
- Evaluation of antiproliferative activities and apoptosis induction caused by copper(II)-benzothiazolesulfonamide complexes in Jurkat T lymphocytes and Caco-2 cells.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2008Article
- Genomewide expression profiling of cryptolepine-induced toxicity in Saccharomyces cerevisiae.Antimicrobial agents and chemotherapy · 2008Article
- Detection of Adriamycin-DNA adducts by accelerator mass spectrometry at clinically relevant Adriamycin concentrations.Nucleic acids research · 2008Article
- Regulation of p53 target gene expression by peptidylarginine deiminase 4.Molecular and cellular biology · 2008Article
- Selective inhibition of yeast regulons by daunorubicin: a transcriptome-wide analysis.BMC genomics · 2008Article
- Susceptibility loci involved in cisplatin-induced cytotoxicity and apoptosis.Pharmacogenetics and genomics · 2008Article
- Mapping genes that contribute to daunorubicin-induced cytotoxicity.Cancer research · 2007Article
- A new bisintercalating anthracycline with picomolar DNA binding affinity.Journal of medicinal chemistry · 2005Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We used a human cDNA macroarray containing various oncogenes and tumour suppressor genes to assess gene expression profiles in early-passage Jurkat T lymphocytes treated with clinically relevant concentrations of the antitumour antibiotic daunorubicin. Several oncogenes and tumour suppressor genes were either up- or down-regulated depending on the daunorubicin concentration used. The expression levels of some of these genes were confirmed by semi-quantitative reverse transcriptase-PCR. We also compared the changes in cell-cycle distribution and the apoptotic morphological characteristics of the cells treated with daunorubicin, using flow cytometry and fluorescence microscopy. Exposure to 182 nM daunorubicin (its IC(75) in Jurkat T cells: where IC(75) is the drug concentration that inhibits growth by 75%) resulted in cell-cycle arrest in G(1) and almost immediate apoptosis. In contrast, decreasing the drug concentration to 91 nM (close to the IC(50)) caused G(2) arrest and cell senescence-like growth arrest, whereas features of apoptosis and necrosis appeared only after longer incubation times. Gene expression profiles, cell-cycle distribution, the presence of DNA damage and the time-dependent response of Jurkat T cells to cell death were correlated clearly. The general behaviour of the genes suggests that cell-cycle arrest and cell death follow distinct pathways depending on drug concentration.
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