ArticleScientific reports2018
ADAM-like Decysin-1 (ADAMDEC1) is a positive regulator of Epithelial Defense Against Cancer (EDAC) that promotes apical extrusion of RasV12-transformed cells.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Epithelial guardians against cancer: integrating cell competition and extrusion in early tumor control.Discover oncology · 2025Review
- A transcriptome-wide association study integrating multi-omics bioinformatics and Mendelian randomization reveals the prognostic value of ADAMDEC1 in colon cancer.Archives of toxicology · 2025Article
- Knockdown of ADAMDEC1 ameliorates ox-LDL-induced endothelial cell injury and atherosclerosis progression.Functional & integrative genomics · 2023Article
- Pleiotropic effects of cell competition between normal and transformed cells in mammalian cancers.Journal of cancer research and clinical oncology · 2023Review
- Elevated ADAM-like Decysin-1 (ADAMDEC1) expression is associated with increased chemo-sensitivity and improved prognosis in breast cancer patients.Annals of translational medicine · 2023Article
- Article
- Article
- Understanding seasonal weight loss tolerance in dairy goats: a transcriptomics approach.BMC genomics · 2020Article
- Symmetry Breaking and Epithelial Cell Extrusion.Cells · 2020Review
- ADAMDEC1 Maintains a Growth Factor Signaling Loop in Cancer Stem Cells.Cancer discovery · 2019Article
- Potential early clinical stage colorectal cancer diagnosis using a proteomics blood test panel.Clinical proteomics · 2019Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have revealed that newly emerging transformed cells are often eliminated from epithelia via cell competition with the surrounding normal epithelial cells. However, it remains unknown whether and how soluble factors are involved in this cancer preventive phenomenon. By performing stable isotope labeling with amino acids in cell culture (SILAC)-based quantitative mass spectrometric analyses, we have identified ADAM-like Decysin-1 (ADAMDEC1) as a soluble protein whose expression is upregulated in the mix culture of normal and RasV12-transformed epithelial cells. Expression of ADAMDEC1 is elevated in normal epithelial cells co-cultured with RasV12 cells. Knockdown of ADAMDEC1 in the surrounding normal cells substantially suppresses apical extrusion of RasV12 cells, suggesting that ADAMDEC1 secreted by normal cells positively regulate the elimination of the neighboring transformed cells. In addition, we show that the metalloproteinase activity of ADAMDEC1 is dispensable for the regulation of apical extrusion. Furthermore, ADAMDEC1 facilitates the accumulation of filamin, a crucial regulator of Epithelial Defense Against Cancer (EDAC), in normal cells at the interface with RasV12 cells. This is the first report demonstrating that an epithelial intrinsic soluble factor is involved in cell competition in mammals.
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