ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Mithramycin is a gene-selective Sp1 inhibitor that identifies a biological intersection between cancer and neurodegeneration.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 93 papers.
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Who cites it
93 citing papers in PubMed, 141 citations in OpenAlex.
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- Exploring the oncogenic roles of T-box transcription factor TBX2 and its potential as a therapeutic target.Biochemical Society transactions · 2025Review
- The Elevated Expression of ORF75, a Lytic KSHV Gene, in Kaposi Sarcoma Lesions is Driven by a GC-rich DNA cis Element in its Promoter Region.bioRxiv : the preprint server for biology · 2024Article
- Induction of AML cell differentiation using HOXA9/DNA binding inhibitors as a potential therapeutic option for HOXA9-dependent AML.HemaSphere · 2024Article
- Docking and molecular dynamic simulations of Mithramycin-A and Tolfenamic acid against Sp1 and survivin.Process biochemistry (Barking, London, England) · 2024Article
- MYC: there is more to it than cancer.Frontiers in cell and developmental biology · 2024Review
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- Prosthetic vascular grafts engineered to combat calcification: Progress and future directions.Biotechnology and bioengineering · 2023Review
- The Cancer/Testis Antigen CT45A1 Promotes Transcription of OncogenicJournal of breast cancer · 2023Article
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- Oncofetal protein IGF2BP1 regulates IQGAP3 expression to maintain stem cell potential in cancer.iScience · 2022Article
- Differential Impact of Random GC Tetrad Binding and Chromatin Events on Transcriptional Inhibition by Olivomycin A.International journal of molecular sciences · 2022Article
33 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
17 authors at 5 institutions in 1 country.
Funding
Abstract
Oncogenic transformation of postmitotic neurons triggers cell death, but the identity of genes critical for degeneration remain unclear. The antitumor antibiotic mithramycin prolongs survival of mouse models of Huntington's disease in vivo and inhibits oxidative stress-induced death in cortical neurons in vitro. We had correlated protection by mithramycin with its ability to bind to GC-rich DNA and globally displace Sp1 family transcription factors. To understand how antitumor drugs prevent neurodegeneration, here we use structure-activity relationships of mithramycin analogs to discover that selective DNA-binding inhibition of the drug is necessary for its neuroprotective effect. We identify several genes (Myc, c-Src, Hif1α, and p21(waf1/cip1)) involved in neoplastic transformation, whose altered expression correlates with protective doses of mithramycin or its analogs. Most interestingly, inhibition of one these genes, Myc, is neuroprotective, whereas forced expression of Myc induces Rattus norvegicus neuronal cell death. These results support a model in which cancer cell transformation shares key genetic components with neurodegeneration.
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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.