ArticleClinical & experimental metastasis2002
MMTV-associated transcription factor binding sites increase nm23-H1 metastasis suppressor gene expression in human breast carcinoma cell lines.
Article in Clinical & experimental metastasis, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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.
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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
18 citing papers in PubMed, 39 citations in OpenAlex.
- A phase II study of medroxyprogesterone acetate in patients with hormone receptor negative metastatic breast cancer: translational breast cancer research consortium trial 007.Breast cancer research and treatment · 2014Trial
- Nonmetastatic cell 1 gene polymorphisms are associated with the clinical progression and prognoses of patients with colorectal cancer.Frontiers in genetics · 2025Article
- RGS19 upregulates Nm23-H1/2 metastasis suppressors by transcriptional activation via the cAMP/PKA/CREB pathway.Oncotarget · 2017Article
- Association between nm23 gene polymorphisms and the risk of endometriosis.Biomedical reports · 2015Article
- Progress on Nme (NDP kinase/Nm23/Awd) gene family-related functions derived from animal model systems: studies on development, cardiovascular disease, and cancer metastasis exemplified.Naunyn-Schmiedeberg's archives of pharmacology · 2015Article
- Metastasis suppressor genes.Histology and histopathology · 2013Review
- Metastasis-suppressor genes in clinical practice: lost in translation?Nature reviews. Clinical oncology · 2011Review
- Metastasis suppressor genes at the interface between the environment and tumor cell growth.International review of cell and molecular biology · 2011Review
- Clinical-translational strategies for the elevation of Nm23-H1 metastasis suppressor gene expression.Molecular and cellular biochemistry · 2009Article
- Learning therapeutic lessons from metastasis suppressor proteins.Nature reviews. Cancer · 2009Review
- Clinical-translational approaches to the Nm23-H1 metastasis suppressor.Clinical cancer research : an official journal of the American Association for Cancer Research · 2008Review
- Genetic polymorphisms of metastasis suppressor gene NME1 and breast cancer survival.Clinical cancer research : an official journal of the American Association for Cancer Research · 2008Article
- Metastasis suppressors and their roles in breast carcinoma.Journal of mammary gland biology and neoplasia · 2007Review
- Translational approaches using metastasis suppressor genes.Journal of bioenergetics and biomembranes · 2006Review
- Metastasis suppressor proteins: discovery, molecular mechanisms, and clinical application.Clinical cancer research : an official journal of the American Association for Cancer Research · 2006Review
- Basic and translational advances in cancer metastasis: Nm23.Journal of bioenergetics and biomembranes · 2003Review
- Inhibition of signal transduction by the nm23 metastasis suppressor: possible mechanisms.Clinical & experimental metastasis · 2003Review
- The glucocorticoid receptor signalling in breast cancer.Journal of cellular and molecular medicineReview
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We hypothesize that elevation of nm23-HI metastasis suppressor gene expression in micrometastatic tumor cells may reduce their subsequent colonization and invasion, and induce differentiation, with a clinical benefit. This report presents the first analysis of the nm23-HI promoter to identify sites which can increase its transcription. Deletion mapping of a 2.1 kb nm23-H1 promoter fragment tethered to a reporter gene identified three regions involved in its differential expression levels among a panel of human breast carcinoma cell lines: a 195 bp NheI-XbaI fragment responsible for basal expression levels, a 248 bp AvrII-Nhel fragment which contributed to the elevated nm23-H1 expression observed in the high expressing cell lines, and a 544 bp AvrII fragment containing an inhibitory element. Examination of the 248 bp AvrII-NheI fragment revealed the unexpected presence of three transcription factor binding sites (MAF/Ets, CTF/NF1 half site and ACAAAG enhancer) previously identified in the MMTV-LTR, and in WAP and milk gene promoters, proposed to mediate mammary-specific gene expression. Mutation of the three sites, individually or together, resulted in two-fold reductions in reporter gene expression. As controls, the same panel of mutations caused a different pattern of reporter gene expression in a non-mammary cell line, and mutation of another nearby site was without effect on nm23-HI. Our data identify a complex regulatory pattern for nm23-H1 transcription, and suggest that a mammary-specific cassette of transcription factors contribute to its elevated expression
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