p53 activates expression of HIC-1, a new candidate tumour suppressor gene on 17p13.3
Abstract
For several human tumour types, allelic loss data suggest that one or more tumour suppressor genes reside telomeric to the p53 gene at chromosome 17p13.1. In the present study we have used a new strategy, involving molecular analysis of a DNA site hypermethylated in tumour DNA, to identify a candidate gene in this region (17p13.3). Our approach has led to identification of HIC-1 (hypermethylated in cancer), a new zinc-finger transcription factor gene which is ubiquitously expressed in normal tissues, but underexpressed in different tumour cells where it is hypermethylated. Multiple characteristics of this gene, including the presence of a p53 binding site in the 5' flanking region, activation of the gene by expression of a wild-type p53 gene and suppression of G418 selectability of cultured brain, breast and colon cancer cells following insertion of the gene, make HIC-1 gene a strong candidate for a tumour suppressor gene in region 17p13.3.
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AV EPDCs express factors associated with EMT, along with unique genes like Hic1.
“AV EPDCs express a variety of factors associated with EMT, along with some unique genes, like Hic1, a tumour suppressor62 and biomarker of adult mesenchymal progenitors63,76.”
From Cell diversity and plasticity during atrioventricular heart valve EMTs (2023) · cites this paper as [62]
Hic1 is a tumour suppressor and biomarker of adult mesenchymal progenitors.
“like Hic1, a tumour suppressor62 and biomarker of adult mesenchymal progenitors63,76.”
From Cell diversity and plasticity during atrioventricular heart valve EMTs (2023) · cites this paper as [62]
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- Authors
- Wales, M. M., Biel, M. A., Deiry, W. E., Nelkin, B. D., Issa, J.-P., Cavenee, W. K., Kuerbitz, S. J., & Baylin, S. B.
- Affiliations
- Johns Hopkins University (US)
- University of California San Diego (US)
- Venue
- Nature Medicine
- Published
- 1995-06
- Volume
- 1
- Issue
- 6
- Pages
- 570-577
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W1966971933
- Cited by
- 421
- References
- 51
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 3 · 2023: 9 · 2022: 8 · 2021: 7 · 2020: 7 · 2019: 4 · 2018: 8 · 2017: 5 · 2016: 14 · 2015: 5 · 2014: 15 · 2013: 14 · 2012: 21
- FWCI
- 9.49
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (R01CA043318, R01CA43318)
- National Institute of General Medical Sciences (T32GM007814, GM-07814)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mechanisms of cancer metastasis
- Keywords
- p53, tumor suppressor, chromosome 17p13.3, DNA hypermethylation, zinc finger transcription factor, p53 binding sites, gene expression regulation, loss of heterozygosity, brain cancer, breast cancer, colon cancer, G418 resistance
- MeSH terms
- Amino Acid Sequence, Brain Neoplasms, Breast Neoplasms, Cell Division, Chromosomes, Human, Pair 17, Colonic Neoplasms, Female, Fibroblasts, Gene Expression Regulation, Growth Inhibitors, Humans, Lung Neoplasms, Methylation, Molecular Sequence Data, Organ Specificity, Recombinant Proteins, Transcription Factors, Transfection, Tumor Cells, Cultured, Gene Expression Regulation, Neoplastic, Genes, Tumor Suppressor, Tumor Suppressor Protein p53, Zinc Fingers, Sequence Alignment, CpG Islands, Kruppel-Like Transcription Factors
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