ArticleThe Journal of biological chemistry2005
Molecular mechanism of inhibition of survivin transcription by the GC-rich sequence-selective DNA binding antitumor agent, hedamycin: evidence of survivin down-regulation associated with drug sensitivity.
Article in The Journal of biological chemistry, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 83 citations in OpenAlex.
- [Comprehensive analytical chemistry experiment： analysis of non-covalent interactions between double-stranded deoxyribonucleic acid and a natural drug by electrospray ionization mass spectrometry].Se pu = Chinese journal of chromatography · 2025Article
- Different DNA Binding and Damage Mode between Anticancer Antibiotics Trioxacarcin A and LL-D49194α1.JACS Au · 2024Article
- Transcription factors specificity protein and nuclear receptor 4A1 in pancreatic cancer.World journal of gastroenterology · 2021Review
- Subcellular Compartmentalization of Survivin is Associated with Biological Aggressiveness and Prognosis in Prostate Cancer.Scientific reports · 2020Article
- Understanding the Role of the Transcription Factor Sp1 in Ovarian Cancer: from Theory to Practice.International journal of molecular sciences · 2020Review
- Inhibition of Specificity Protein 1 Is Involved in Phloretin-Induced Suppression of Prostate Cancer.BioMed research international · 2020Article
- Role of Sp1 expression in gastric cancer: A meta-analysis and bioinformatics analysis.Oncology letters · 2019Article
- Cancer therapeutics using survivin BIRC5 as a target: what can we do after over two decades of study?Journal of experimental & clinical cancer research : CR · 2019Review
- Synthesis of novel 10,11-methylenedioxy-camptothecin glycoside derivatives and investigation of their anti-tumor effectsRSC advances · 2019Article
- Camptothecin (CPT) and its derivatives are known to target topoisomerase I (Top1) as their mechanism of action: did we miss something in CPT analogue molecular targets for treating human disease such as cancer?American journal of cancer research · 2017Review
- Synergistic effect of allyl isothiocyanate (AITC) on cisplatin efficacy in vitro and in vivo.American journal of cancer research · 2015Article
- An intravenous (i.v.) route-compatible formulation of FL118, a survivin, Mcl-1, XIAP, and cIAP2 selective inhibitor, improves FL118 antitumor efficacy and therapeutic index (TI).American journal of translational research · 2013Article
- Drugging the undruggable: transcription therapy for cancer.Biochimica et biophysica acta · 2013Review
- Transcriptional inhibition of p21WAF1/CIP1 gene (CDKN1) expression by survivin is at least partially p53-dependent: evidence for survivin acting as a transcription factor or co-factor.Biochemical and biophysical research communications · 2012Article
- Article
- Suppression of survivin promoter activity by YM155 involves disruption of Sp1-DNA interaction in the survivin core promoter.International journal of biochemistry and molecular biology · 2012Article
- Inhibition of pituitary tumor-transforming gene-1 in thyroid cancer cells by drugs that decrease specificity proteins.Molecular carcinogenesis · 2011Article
- The Apoptotic Effect of the Hexane Extract of Rheum undulatum L. in Oral Cancer Cells through the Down-regulation of Specificity Protein 1 and Survivin.Laboratory animal research · 2011Article
- Cooperative and individualistic functions of the microRNAs in the miR-23a~27a~24-2 cluster and its implication in human diseases.Molecular cancer · 2010Review
- Inactivation of the orphan nuclear receptor TR3/Nur77 inhibits pancreatic cancer cell and tumor growth.Cancer research · 2010Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Expression of the antiapoptotic protein survivin is associated with cancer cell viability and drug resistance. Thus, control of its expression in cancer cells has significant consequences for cancer therapeutics. Here we have shown that hedamycin, a GC-rich DNA binding drug, down-regulated survivin expression. Using a series of survivin promoter-luciferase constructs, we have identified an 86-bp GC-rich DNA element (-124 to -39) that mediates the ability of hedamycin to down-regulate survivin expression. Furthermore, both in vivo foot-printing and in vitro gel mobility shift experiments revealed that hedamycin bound to a 21-bp GC-rich DNA element (-115 to -95) in the survivin promoter. This drug-DNA interaction abrogated the binding of Sp-1 or Sp1-like proteins to the 21-bp cis-acting DNA element, and mutagenesis of this region consistently diminished survivin promoter activity. Finally, down-regulation of survivin transcription by hedamycin modulated the viability of cancer cells. These data suggest that abrogation of Sp-1 or Sp1-like protein binding to the 21-bp DNA element in the survivin promoter contributes at least in part to the inhibitory effect of hedamycin on survivin gene transcription. Drug-induced modulation of survivin gene expression may provide novel approaches for cancer therapeutics.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.