ArticleCell proliferation2011
Mithramycin reduces expression of fibro-proliferative mRNAs in human gingival fibroblasts.
Article in Cell proliferation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 13 citations in OpenAlex.
- Integrative analysis of transcriptome, DNA methylome, and chromatin accessibility reveals candidate therapeutic targets in hypertrophic cardiomyopathy.Protein & cell · 2024Article
- Interaction and Collaboration of SP1, HIF-1, and MYC in Regulating the Expression of Cancer-Related Genes to Further Enhance Anticancer Drug Development.Current issues in molecular biology · 2023Review
- Heterologous reconstitution of the biosynthesis pathway for 4-demethyl-premithramycinone, the aglycon of antitumor polyketide mithramycin.Microbial cell factories · 2020Article
- TGFβ upregulates PAR-1 expression and signalling responses in A549 lung adenocarcinoma cells.Oncotarget · 2016Article
- A novel mithramycin analogue with high antitumor activity and less toxicity generated by combinatorial biosynthesis.Journal of medicinal chemistry · 2012Article
- Loss of PPARγ expression by fibroblasts enhances dermal wound closure.Fibrogenesis & tissue repair · 2012Article
- Sp1king out cancer (....and fibrosis?).Journal of cell communication and signaling · 2012Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Fibrosis is characterized by loss of normal structure and function of a tissue or organ resulting from excessive fibroblast proliferation and extracellular matrix production. Currently, there is no efficient treatment for fibrosis. Herein, we test effects of the drug mithramycin, which targets the Sp1 family of transcription factors, on mRNA expression by human gingival fibroblasts. Mithramycin reduced expression of connective tissue growth factor and type I collagen mRNAs. Microarray profiling revealed that mithramycin selectively blocked expression of cell proliferation and transforming growth factor-beta (TGF-β) signalling clusters. These microarray data were validated using real-time polymerase chain reaction and western blot analyses. Mithramycin suppressed expression of key profibrotic TGF-β signalling mediators, Smad3 and p300, as well as cell proliferation. Taken together, these data suggest that the Sp1 family of transcription factors may contribute to expression of fibrogenic genes in human gingival fibroblasts; drugs targeting the Sp1 family may be beneficial in treatment of fibro-proliferative diseases.
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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.