ArticlePigment cell & melanoma research2010
Smad7 restricts melanoma invasion by restoring N-cadherin expression and establishing heterotypic cell-cell interactions in vivo.
Article in Pigment cell & melanoma research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 28 citations in OpenAlex.
- Androgen drives melanoma invasiveness and metastatic spread by inducing tumorigenic fucosylation.Nature communications · 2024Article
- Employing CRISPR-Cas9 to Generate CD133 Synthetic Lethal Melanoma Stem Cells.International journal of molecular sciences · 2022Article
- CRISPR-Cas9 Knockdown and Induced Expression of CD133 Reveal Essential Roles in Melanoma Invasion and Metastasis.Cancers · 2019Article
- SOX7 co-regulates Wnt/β-catenin signaling with Axin-2: both expressed at low levels in breast cancer.Scientific reports · 2016Article
- The role of Smad7 in oral mucositis.Protein & cell · 2015Review
- N-cadherin participated in invasion and metastasis of human esophageal squamous cell carcinoma via taking part in the formation of vasculogenic mimicry.Medical oncology (Northwood, London, England) · 2015Article
- Id2, Id3 and Id4 overcome a Smad7-mediated block in tumorigenesis, generating TGF-β-independent melanoma.Carcinogenesis · 2014Article
- Transforming growth factor β signaling overcomes dasatinib resistance in lung cancer.PloS one · 2014Article
- The dual role of Smad7 in the control of cancer growth and metastasis.International journal of molecular sciences · 2013Review
- Insights into the Transforming Growth Factor-β Signaling Pathway in Cutaneous Melanoma.Annals of dermatology · 2013Article
- Wnt/beta-catenin signaling and small molecule inhibitors.Current pharmaceutical design · 2013Review
- Expression of microphthalmia-associated transcription factor (MITF), which is critical for melanoma progression, is inhibited by both transcription factor GLI2 and transforming growth factor-β.The Journal of biological chemistry · 2012Article
- TGF-beta-RI kinase inhibitor SD-208 reduces the development and progression of melanoma bone metastases.Cancer research · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
The list of transforming growth factor-beta (TGF-β)-related proteins in non-canonical TGF-β signaling is growing. Examples include receptor-Smads directing micro-RNA processing and inhibitory-Smads, e.g. Smad7, directing cell adhesion. Human skin grafts with fluorescently tagged melanoma cells revealed Smad7-expressing cells positioned themselves proximal to the dermal-epidermal junction and failed to form tumors, while control cells readily invaded and formed tumors within the dermis. Smad7 significantly inhibited β-catenin T41/S45 phosphorylation associated with degradation and induced a 4.5-fold increase in full-length N-cadherin. Cell adhesion assays confirmed a strong interaction between Smad7-expressing cells and primary dermal fibroblasts mediated via N-cadherin, while control cells were incapable of such interaction. Immunofluorescent analysis of skin grafts indicated N-cadherin homotypic interaction at the surface of both Smad7 cells and primary dermal fibroblasts, in contrast to control melanoma cells. We propose that Smad7 suppresses β-catenin degradation and promotes interaction with N-cadherin, stabilizing association with neighboring dermal fibroblasts, thus mitigating invasion.
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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.