ArticleClinical medicine. Oncology2008
Signal transduction involving the dmp1 transcription factor and its alteration in human cancer.
Article in Clinical medicine. Oncology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Stabilization of the p53-DNA Complex by the Nuclear Protein Dmp1α.Cancer investigation · 2017Article
- Novel Molecular Markers for Breast Cancer.Biomarkers in cancer · 2016Review
- Clinical applications of mouse models for breast cancer engaging HER2/neu.Integrative cancer science and therapeutics · 2016Article
- Human DMTF1β antagonizes DMTF1α regulation of the p14(ARF) tumor suppressor and promotes cellular proliferation.Biochimica et biophysica acta · 2015Article
- Aberrant expression of cyclin D1 in cancer.Signal transduction insights · 2015Article
- Alterations of p63 and p73 in human cancers.Sub-cellular biochemistry · 2014Review
- Dmp1α inhibits HER2/neu-induced mammary tumorigenesis.PloS one · 2013Article
- Transgenic and knockout mice models to reveal the functions of tumor suppressor genes.Clinical Medicine Insights. Oncology · 2011Article
- Classical and Novel Prognostic Markers for Breast Cancer and their Clinical Significance.Clinical Medicine Insights. Oncology · 2010Article
- The Arf-inducing transcription factor Dmp1 encodes a transcriptional activator of amphiregulin, thrombospondin-1, JunB and Egr1.International journal of cancer · 2010Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Dmp1 (cyclin D-interacting myb-like protein 1; also called Dmtf1) is a transcription factor that has been isolated in a yeast two-hybrid screen through its binding property to cyclin D2. Dmp1 directly binds to and activates the Arf promoter and induces Arf-p53-dependent cell cycle arrest in primary cells. D-type cyclins usually inhibit Dmp1-mediated transcription in a Cdk-independent fashion; however, Dmp1 shows synergistic effects with D-cyclins on the Arf promoter. Ras or Myc oncogene-induced tumor formation is accelerated in both Dmp1(+/-) and Dmp1(-/-) mice with no significant differences between Dmp1(+/-) and Dmp1(-/-). Thus, Dmp1 is haplo-insufficient for tumor suppression. Tumors from Dmp1(-/-) or Dmp1(+/-) mice often retain wild-type Arf and p53, suggesting that Dmp1 is a physiological regulator of the Arf-p53 pathway. The Dmp1 promoter is activated by oncogenic Ras-Raf signaling, while it is repressed by physiological mitogenic stimuli, overexpression of E2F proteins, and genotoxic stimuli mediated by NF-κB. The human DMP1 gene (hDMP1) is located on chromosome 7q21 and is hemizygously deleted in approximately 40% of human lung cancers, especially those that retain normal INK4a/ARF and P53 loci. Thus, hDMP1 is clearly involved in human carcinogenesis, and tumors with hDMP1 deletion may constitute a discrete disease entity.
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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.