ArticleOncogene1999
Silencing of metallothionein-I gene in mouse lymphosarcoma cells by methylation.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 45 citations in OpenAlex.
- A host-directed oxadiazole compound potentiates antituberculosis treatment via zinc poisoning in human macrophages and in a mouse model of infection.PLoS biology · 2024Article
- CpG Site-Specific Regulation of Metallothionein-1 Gene Expression.International journal of molecular sciences · 2020Article
- Maternal dietary zinc supplementation enhances the epigenetic-activated antioxidant ability of chick embryos from maternal normal and high temperatures.Oncotarget · 2017Article
- The Functions of Metallothionein and ZIP and ZnT Transporters: An Overview and Perspective.International journal of molecular sciences · 2016Review
- Environmental chemicals and DNA methylation in adults: a systematic review of the epidemiologic evidence.Clinical epigenetics · 2015Review
- Hypothermia enhances induction of protective protein metallothionein under ischemia.Journal of neuroinflammation · 2013Article
- USF-1 is critical for maintaining genome integrity in response to UV-induced DNA photolesions.PLoS genetics · 2012Article
- Article
- Loss of metallothionein predisposes mice to diethylnitrosamine-induced hepatocarcinogenesis by activating NF-kappaB target genes.Cancer research · 2010Article
- A new class of quinoline-based DNA hypomethylating agents reactivates tumor suppressor genes by blocking DNA methyltransferase 1 activity and inducing its degradation.Cancer research · 2009Article
- Methylation and silencing of protein tyrosine phosphatase receptor type O in chronic lymphocytic leukemia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2007Article
- Article
- Physical and functional interaction of DNA methyltransferase 3A with Mbd3 and Brg1 in mouse lymphosarcoma cells.Cancer research · 2005Article
- Peptide mass mapping of acetylated isoforms of histone H4 from mouse lymphosarcoma cells treated with histone deacetylase (HDACs) inhibitors.Journal of the American Society for Mass Spectrometry · 2005Article
- Article
- Protein tyrosine phosphatase receptor-type O (PTPRO) exhibits characteristics of a candidate tumor suppressor in human lung cancer.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Suppression of the protein tyrosine phosphatase receptor type O gene (PTPRO) by methylation in hepatocellular carcinomas.Oncogene · 2003Article
- Inhibitors of histone deacetylase and DNA methyltransferase synergistically activate the methylated metallothionein I promoter by activating the transcription factor MTF-1 and forming an open chromatin structure.Molecular and cellular biology · 2002Article
- Suppression of metallothionein-I/II expression and its probable molecular mechanisms.Environmental health perspectives · 2002Article
- Role of de novo DNA methyltransferases and methyl CpG-binding proteins in gene silencing in a rat hepatoma.The Journal of biological chemistry · 2002Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Metallothionein-I (MT-I) gene is silenced by methylation of CpG islands in mouse lymphosarcoma P1798 cells but not in the thymus, the cell type from which the tumor was derived. Bisulfite genomic sequencing revealed that all 21 CpG dinucleotides present within -216 bp to +1 bp with respect to transcription start site are methylated in the tumor cell line, but none is methylated in the thymus. The lymphosarcoma cells induced MT-I in response to heavy metals only after demethylation with 5-azacytidine (5-AsaC). The electrophoretic mobility shift assay using specific oligonucleotide probes showed that the key transcription factors regulating MT-I gene (e.g., MTF-1, Sp 1 and MLTF/USF) are active in P1798 cells. In vivo footprinting of the proximal promoter region showed that none of the metal regulatory elements (MREs) or MLTF/USF are occupied in response to heavy metals. Demethylation of the lymphosarcoma cells with 5-AzaC resulted in constitutive footprinting at MLTF/ARE, and zinc-inducible footprinting at MRE-c, MRE-d and MRE-e sites. Demethylation of just 10-20% of the CpG islands was sufficient to render the gene inducible by cadmium or zinc. The MT-I induction persisted in the cancer cells for several generations even after withdrawal of 5-AzaC from the culture medium.
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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.