ArticleThe American journal of pathology2007
Snai2 expression enhances ultraviolet radiation-induced skin carcinogenesis.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Vimentin Suppresses Inflammation and Tumorigenesis in the Mouse Intestine.Frontiers in cell and developmental biology · 2022Article
- The transcription factor Slug represses p16Nature communications · 2019Article
- Identifying global expression patterns and key regulators in epithelial to mesenchymal transition through multi-study integration.BMC cancer · 2017Article
- Role of the Slug Transcription Factor in Chemically-Induced Skin Cancer.Journal of clinical medicine · 2016Article
- Development and Characterization of a Novel in vitro Progression Model for UVB-Induced Skin Carcinogenesis.Scientific reports · 2015Article
- Loss of Snail2 favors skin tumor progression by promoting the recruitment of myeloid progenitors.Carcinogenesis · 2015Article
- Loss of keratinocytic RXRα combined with activated CDK4 or oncogenic NRAS generates UVB-induced melanomas via loss of p53 and PTEN in the tumor microenvironment.Molecular cancer research : MCR · 2015Article
- The oncogenic GLI transcription factors facilitate keratinocyte survival and transformation upon exposure to genotoxic agents.Oncogene · 2014Article
- Slug expression in mouse skin and skin tumors is not regulated by p53.The Journal of investigative dermatology · 2014Article
- Src is activated by the nuclear receptor peroxisome proliferator-activated receptor β/δ in ultraviolet radiation-induced skin cancer.EMBO molecular medicine · 2014Article
- The mesenchymal-epithelial transition during in vitro decidualization.Reproductive sciences (Thousand Oaks, Calif.) · 2013Article
- The skinny on Slug.Molecular carcinogenesis · 2010Review
- Cutaneous wound reepithelialization is compromised in mice lacking functional Slug (Snai2).Journal of dermatological science · 2009Article
- E-cadherin, fibronectin and Slug immunoexpression in non-melanoma skin cancers.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologieArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Snai2, encoded by the SNAI2 gene, has been shown to modulate epithelial-mesenchymal transformation (EMT), the conversion of sessile epithelial cells attached to adjacent cells and to the basement membrane into dissociated and motile fibroblastic cells. EMT occurs during development, wound healing, and carcinoma progression. Using Snai2-null mice (Snai2(lacZ)), we evaluated the role of Snai2 in UV radiation (UVR)-induced skin carcinogenesis. In chronically UVR-exposed nontumor-bearing skin from Snai2-null mice, inflammation and epidermal proliferation were decreased compared with wild-type (+/+) skin. Snai2-null mice had a consistently lower tumor burden than +/+ mice. In addition, null mice developed fewer aggressive spindle cell tumors, believed to arise from squamous cell carcinomas that have undergone EMT, than +/+ mice; however, the difference in tumor type distribution between the two genotypes was not statistically significant. No metastases were observed in either the +/+ or Snai2-null mice. Using quantitative reverse transcriptase-polymerase chain reaction and immunohistochemistry, we showed that the spindle cell tumors in the Snai2-null mice demonstrated impaired EMT, as shown by decreased vimentin and increased cadherin 1 expression. This study confirms a role for Snai2 in EMT, but demonstrates that Snai2 expression is not required for the development or progression of UVR-induced skin tumors.
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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.