ArticleMolecular cancer2016
MiR-204 silencing in intraepithelial to invasive cutaneous squamous cell carcinoma progression.
Article in Molecular cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 54 citations in OpenAlex.
- Review
- Cavin gene family and caveolae-related disorders: pathogenetic roles and possible mechanisms.Cell communication and signaling : CCS · 2026Review
- EWS::FLI1 expression in human embryonic mesenchymal stem cells leads to transcriptional reprograming, defective DNA damage repair and Ewing sarcoma.Nature communications · 2025Article
- From actinic keratosis to cutaneous squamous cell carcinoma: the key pathogenesis and treatments.Frontiers in immunology · 2025Review
- Micro RNA Dysregulation in Keratinocyte Carcinomas: Clinical Evidence, Functional Impact, and Future Directions.International journal of molecular sciences · 2024Review
- Article
- miR-204 suppresses uveal melanoma cell migration and invasion through negative regulation of RAB22A.Functional & integrative genomics · 2023Article
- miRNA in Molecular Diagnostics.Bioengineering (Basel, Switzerland) · 2022Review
- miR-204-5p in vivo inhibition cause diminished CD45RO cells rate in lungs of melanoma B16-bearing mice.Non-coding RNA research · 2022Article
- Low expression of microRNA-125b enhances the expression of STAT3 and contributes to cholesteatoma growth.Archives of medical science : AMS · 2022Article
- Non-coding RNAs in skin cancers:Biological roles and molecular mechanisms.Frontiers in pharmacology · 2022Review
- Critical roles of PTPN family members regulated by non-coding RNAs in tumorigenesis and immunotherapy.Frontiers in oncology · 2022Review
- Oh, the Mutations You'll Acquire! A Systematic Overview of Cutaneous Squamous Cell Carcinoma.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2021Review
- DNA methylation-mediated silencing of microRNA-204 enhances T cell acute lymphoblastic leukemia by up-regulating MMP-2 and MMP-9 via NF-κB.Journal of cellular and molecular medicine · 2021Article
- Review
- Current and Future Trends in Molecular Biomarkers for Diagnostic, Prognostic, and Predictive Purposes in Non-Melanoma Skin Cancer.Journal of clinical medicine · 2020Review
- Deciphering the Molecular Landscape of Cutaneous Squamous Cell Carcinoma for Better Diagnosis and Treatment.Journal of clinical medicine · 2020Review
- The Role of Epithelial-to-Mesenchymal Transition in Cutaneous Squamous Cell Carcinoma : Epithelial-to-Mesenchymal Transition in Cutaneous SCC.Current treatment options in oncology · 2020Review
- Targeted Therapy Against the Cell of Origin in Cutaneous Squamous Cell Carcinoma.International journal of molecular sciences · 2019Review
- MicroRNA Dysregulation in Cutaneous Squamous Cell Carcinoma.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCutaneous squamous cell carcinoma (cSCC) is the second most common skin cancer and frequently progresses from an actinic keratosis (AK), a sun-induced keratinocyte intraepithelial neoplasia (KIN). Epigenetic mechanisms involved in the phenomenon of progression from AK to cSCC remain to be elicited.
methodsExpression of microRNAs in sun-exposed skin, AK and cSCC was analysed by Agilent microarrays. DNA methylation of miR-204 promoter was determined by bisulphite treatment and pyrosequencing. Identification of miR-204 targets and pathways was accomplished in HaCat cells. Immunofluorescence and immunohistochemistry were used to analyze STAT3 activation and PTPN11 expression in human biopsies.
resultscSCCs display a marked downregulation of miR-204 expression when compared to AK. DNA methylation of miR-204 promoter was identified as one of the repressive mechanisms that accounts for miR-204 silencing in cSCC. In HaCaT cells miR-204 inhibits STAT3 and favours the MAPK signaling pathway, likely acting through PTPN11, a nuclear tyrosine phosphatase that is a direct miR-204 target. In non-peritumoral AK lesions, activated STAT3, as detected by pY705-STAT3 immunofluorescence, is retained in the membrane and cytoplasm compartments, whereas AK lesions adjacent to cSCCs display activated STAT3 in the nuclei.
conclusionsOur data suggest that miR-204 may act as a "rheostat" that controls the signalling towards the MAPK pathway or the STAT3 pathway in the progression from AK to cSCC.
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