ArticlePloS one2011
Suppression of breast tumor growth and metastasis by an engineered transcription factor.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 55 citations in OpenAlex.
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- Butyrate mediates anti-inflammatory effects ofGut microbes · 2020Article
- Activating PTEN Tumor Suppressor Expression with the CRISPR/dCas9 System.Molecular therapy. Nucleic acids · 2019Article
- miR-1 inhibits the proliferation of breast cancer stem cells by targeting EVI-1.OncoTargets and therapy · 2018Article
- Waking up dormant tumor suppressor genes with zinc fingers, TALEs and the CRISPR/dCas9 system.Oncotarget · 2016Article
- Writing of H3K4Me3 overcomes epigenetic silencing in a sustained but context-dependent manner.Nature communications · 2016Article
- miR-363 induces transdifferentiation of human kidney tubular cells to mesenchymal phenotype.Clinical and experimental nephrology · 2016Article
- miRNAs Signature in Head and Neck Squamous Cell Carcinoma Metastasis: A Literature Review.Journal of dentistry (Shiraz, Iran) · 2016Review
- Epigenetic Editing: On the Verge of Reprogramming Gene Expression at Will.Current genetic medicine reports · 2016Review
- Prolonged re-expression of the hypermethylated gene EPB41L3 using artificial transcription factors and epigenetic drugs.Epigenetics · 2015Article
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- Expression and localization of maspin in cervical cancer and its role in tumor progression and lymphangiogenesis.Archives of gynecology and obstetrics · 2014Article
- Role of microRNA-1 in human cancer and its therapeutic potentials.BioMed research international · 2014Review
- Functional validation of putative tumor suppressor gene C13ORF18 in cervical cancer by Artificial Transcription Factors.Molecular oncology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Maspin is a tumor and metastasis suppressor playing an essential role as gatekeeper of tumor progression. It is highly expressed in epithelial cells but is silenced in the onset of metastatic disease by epigenetic mechanisms. Reprogramming of Maspin epigenetic silencing offers a therapeutic potential to lock metastatic progression. Herein we have investigated the ability of the Artificial Transcription Factor 126 (ATF-126) designed to upregulate the Maspin promoter to inhibit tumor progression in pre-established breast tumors in immunodeficient mice. ATF-126 was transduced in the aggressive, mesenchymal-like and triple negative breast cancer line, MDA-MB-231. Induction of ATF expression in vivo by Doxycycline resulted in 50% reduction in tumor growth and totally abolished tumor cell colonization. Genome-wide transcriptional profiles of ATF-induced cells revealed a gene signature that was found over-represented in estrogen receptor positive (ER+) "Normal-like" intrinsic subtype of breast cancer and in poorly aggressive, ER+ luminal A breast cancer cell lines. The comparison transcriptional profiles of ATF-126 and Maspin cDNA defined an overlapping 19-gene signature, comprising novel targets downstream the Maspin signaling cascade. Our data suggest that Maspin up-regulates downstream tumor and metastasis suppressor genes that are silenced in breast cancers, and are normally expressed in the neural system, including CARNS1, SLC8A2 and DACT3. In addition, ATF-126 and Maspin cDNA induction led to the re-activation of tumor suppressive miRNAs also expressed in neural cells, such as miR-1 and miR-34, and to the down-regulation of potential oncogenic miRNAs, such as miR-10b, miR-124, and miR-363. As expected from its over-representation in ER+ tumors, the ATF-126-gene signature predicted favorable prognosis for breast cancer patients. Our results describe for the first time an ATF able to reduce tumor growth and metastatic colonization by epigenetic reactivation of a dormant, normal-like, and more differentiated gene program.
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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.