ArticleClinical oral investigations2013
Overexpression of Smad proteins, especially Smad7, in oral epithelial dysplasias.
Article in Clinical oral investigations, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Comprehensive analysis of the TGF-β signaling pathway: molecular mechanisms, disease drivers, and frontiers in clinical translation.Frontiers in immunology · 2026Review
- Protein inhibitor of activated signal transducer and activator of transcription 2 is an oncoprotein in oral squamous cell carcinoma and related to cigarette smoking - An in vitro study.Journal of dental sciences · 2024Article
- Biomarkers of malignant transformation in oral leukoplakia: from bench to bedside.Journal of Zhejiang University. Science. B · 2023Review
- Aberrations in SMAD family of genes among HNSCC patients.Bioinformation · 2021Article
- TRAIL, Wnt, Sonic Hedgehog, TGFβ, and miRNA Signalings Are Potential Targets for Oral Cancer Therapy.International journal of molecular sciences · 2017Review
- Low level laser therapy/photobiomodulation in the management of side effects of chemoradiation therapy in head and neck cancer: part 1: mechanisms of action, dosimetric, and safety considerations.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2016Review
- Role of Smad signaling in kidney disease.International urology and nephrology · 2015Review
- Smad7 regulates compensatory hepatocyte proliferation in damaged mouse liver and positively relates to better clinical outcome in human hepatocellular carcinoma.Clinical science (London, England : 1979) · 2015Article
- Aberrant expression of p-Smad3 in oral carcinogenesis.Clinical oral investigations · 2015Article
- SMAD7: a timer of tumor progression targeting TGF-β signaling.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Review
- Can immunohistochemistry serve as an alternative to subjective histopathological diagnosis of oral epithelial dysplasia?Biomarkers in cancer · 2013Review
- Comparative analysis of TGF-β/Smad signaling dependent cytostasis in human hepatocellular carcinoma cell lines.PloS one · 2013Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTransforming growth factor β, via membrane-bound receptors and downstream Smad2-4, 7, can modulate tumorigenesis. Smad2 and Smad3 heterodimerize with Smad4, and the complex migrates to the nucleus to regulate the expression of target genes. Smad7 is a key negative regulator of this signaling pathway. This study aimed to examine Smad2-4, 7 expression and phosphorylated Smad2-3 (p-Smad2-3) in oral epithelial dysplasia and compared it with normal oral mucosa, hyperkeratosis/epithelial hyperplasia and squamous cell carcinoma (SCC). MATERIALS AND
methodsImmunohistochemical staining of Smad2-4, 7 and p-Smad2-3, was performed for 75 samples of human oral mucosa, including hyperkeratosis/epithelial hyperplasia (n = 20), mild epithelial dysplasia (n = 11), moderate to severe epithelial dysplasia (n = 11), and SCC (n = 43). Normal buccal mucosa samples (n = 9) were also included.
resultsA significant increase in Smad7 expression was observed in the ascending order of samples of normal oral mucosa, hyperkeratosis/epithelial hyperplasia/mild oral epithelial dysplasia, moderate to severe oral epithelial dysplasia, and well-differentiated oral SCC/moderately to poorly differentiated oral SCC. Additionally, significant increases in Smad7 expression were noted as compared with expression of Smad2-4 and p-Smad2-3 in lesions of hyperkeratosis/epithelial hyperplasia, mild oral epithelial dysplasia, moderate to severe oral epithelial dysplasia, well-differentiated oral SCC, and moderately to poorly differentiated oral SCC.
conclusionsOur results indicate that Smad proteins, particularly Smad7, in oral epithelial dysplasia and SCC could contribute to the attenuation of Smads anti-proliferative signaling in cancer development. CLINICAL RELEVANCE: Smad7 could be a marker for risk of malignant transformation of oral epithelial dysplasia.
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