ArticleOncogene2003
Mammary gland development requires syndecan-1 to create a beta-catenin/TCF-responsive mammary epithelial subpopulation.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 56 citations in OpenAlex.
- DHRS2 regulates epithelial-mesenchymal transition in breast cancer cells.Molecular biology reports · 2026Article
- Extracellular matrix remodeling fibroblasts govern the tumor microenvironment disparity between adenomatous lesions and adenocarcinoma in gallbladder.Frontiers in immunology · 2025Article
- Syndecan-1 (CD138), Carcinomas and EMT.International journal of molecular sciences · 2021Review
- HS2ST1-dependent signaling pathways determine breast cancer cell viability, matrix interactions, and invasive behavior.Cancer science · 2020Article
- Three-Dimensional Models as a New Frontier for Studying the Role of Proteoglycans in the Normal and Malignant Breast Microenvironment.Frontiers in cell and developmental biology · 2020Review
- Physiological and anatomical aspects of the reproduction of mice with reduced Syndecan-1 expression.Reproductive biology and endocrinology : RB&E · 2019Article
- Article
- Dually modified transmembrane proteoglycans in development and disease.Cytokine & growth factor reviews · 2018Review
- Alterations in Corneal Sensory Nerves During Homeostasis, Aging, and After Injury in Mice Lacking the Heparan Sulfate Proteoglycan Syndecan-1.Investigative ophthalmology & visual science · 2017Article
- The origin of breast tumor heterogeneity.Oncogene · 2015Review
- Insights into the key roles of proteoglycans in breast cancer biology and translational medicine.Biochimica et biophysica acta · 2015Review
- IGF1R inhibition in mammary epithelia promotes canonical Wnt signaling and Wnt1-driven tumors.Cancer research · 2014Article
- Prognostic significance of RSPO1, WNT1, P16, WT1, and SDC1 expressions in invasive ductal carcinoma of the breast.World journal of surgical oncology · 2013Article
- Syndecans in cartilage breakdown and synovial inflammation.Nature reviews. Rheumatology · 2013Review
- Article
- Use of an in vivo animal model for assessing the role of integrin α(6)β(4) and syndecan-1 in early steps in papillomavirus infection.Virology · 2012Article
- Stage-dependent regulation of mammary ductal branching by heparan sulfate and HGF-cMet signaling.Developmental biology · 2011Article
- Effect of mutant β-catenin on liver growth homeostasis and hepatocarcinogenesis in transgenic mice.Liver international : official journal of the International Association for the Study of the Liver · 2011Article
- Either ZEB1 or ZEB2/SIP1 can play a central role in regulating the Epstein-Barr virus latent-lytic switch in a cell-type-specific manner.Journal of virology · 2010Article
- Loss of the heparan sulfate sulfotransferase, Ndst1, in mammary epithelial cells selectively blocks lobuloalveolar development in mice.PloS one · 2010Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Mice with a null mutation in the cell surface heparan sulfate (HS) proteoglycan, syndecan-1 (Sdc1), develop almost normally, but resist mammary tumor development in response to Wnt-1. Here, we test the hypothesis that Sdc1 promotes Wnt-1-induced tumor development by interacting with the Wnt cell surface signaling complex. Thus, the response of Sdc1-/- mammary epithelial cells (mecs) to the intracellular, activated Wnt signal transducer, DeltaNbeta-catenin, was assayed both in vitro and in vivo, to test whether beta-catenin/TCF transactivation was Sdc1-independent. Surprisingly, we found that the expression of a canonical Wnt pathway reporter, TOP-FLASH, was reduced by 50% in both unstimulated Sdc1-/- mecs and in stimulated cells responding to Wnt1 or DeltaNbeta-catenin. Tumor development in response to DeltaNbeta-catenin was also significantly delayed on a Sdc1-/- background. Furthermore, the average beta-catenin/TCF transactivation per cell was normal in Sdc1-/- mec cultures, but the number of responsive cells was reduced by 50%. Sdc1-/- mecs show compensatory changes that maintain the number of HS chains, hence these experiments cannot test the coreceptor activity of HS for Wnt signaling. We propose that TCF-dependent transactivational activity is suppressed in 50% of cells in Sdc1-/- glands, and conclude that the major effect of Sdc1 does not map to the activity of the Wnt signaling complex, but to another pathway to create or stabilize the beta-catenin/TCF-responsive tumor precursor cells in mouse mammary gland.
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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.