Differential BMI1, TWIST1, SNAI2 mRNA expression pattern correlation with malignancy type in a spectrum of common cutaneous malignancies: basal cell carcinoma, squamous cell carcinoma, and melanoma
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Summary
These findings provide support for the hypothesis that the spectrum of cutaneous cancers could be better understood as a series of gene dosage-dependent entities with distinct molecular events.
- Type
- article
- Published
- 2017-04-01
- Cited by
- 13
- References
- 34
- OpenAlex
- https://openalex.org/W2528301979
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:21474392
Keywords
BMI1, Melanoma, Basal cell carcinoma, Medicine, Cancer
References
- UV damage and DNA repair in malignant melanoma and nonmelanoma skin cancer.
- SNAI2 Controls the Undifferentiated State of Human Epidermal Progenitor Cells
- Linkage between Twist1 and Bmi1: Molecular mechanism of cancer metastasis/stemness and clinical implications
- Expression of RUNX3 in skin cancers
- Cancer stem cells and epithelial–mesenchymal transition: Concepts and molecular links
- Loss of BMI-1 expression is associated with clinical progress of malignant melanoma
- Different levels of Twist1 regulate skin tumor initiation, stemness, and progression.
- The epigenetics of epithelial-mesenchymal plasticity in cancer
- p16 gene expression in basal cell carcinoma.
- Normal and disease-related biological functions of Twist1 and underlying molecular mechanisms
- Oncogene-induced senescence
- Consistent expression of the stem cell renewal factor BMI‐1 in primary and metastatic melanoma
- Transitions between epithelial and mesenchymal states: acquisition of malignant and stem cell traits
- BMI1 and TWIST1 downregulated mRNA expression in basal cell carcinoma.
- Twist is an integrator of SHH, FGF, and BMP signaling
- Bmi1 is essential in Twist1-induced epithelial–mesenchymal transition
- p38 MAPK-Mediated Bmi-1 Down-Regulation and Defective Proliferation in ATM-Deficient Neural Stem Cells Can Be Restored by Akt Activation
- Induction of EMT by twist proteins as a collateral effect of tumor-promoting inactivation of premature senescence.
- Long Noncoding RNA, Polycomb, and the Ghosts Haunting INK4b-ARF-INK4a Expression
- Non-melanoma skin cancer.
Cited by
- Upregulation of SNAI2 and SOX9 mRNA versus downregulation of eight other EMT/stemness related genes in basal cell carcinoma
- Altered expression of E-Cadherin-related transcription factors indicates partial epithelial-mesenchymal transition in aggressive meningiomas.
- Evaluation of expression of genes CADM1, TWIST1 and CDH1 by immunohistochemestry in melanocytic lesions.
- IL‐17A promotes cell migration and invasion of glioblastoma cells via activation of PI3K/AKT signalling pathway
- MiR-33a-5p inhibits the growth and metastasis of melanoma cells by targeting SNAI2.
- Decreased Sox2 Messenger RNA Expression in Basal Cell Carcinoma
- Whole-genome identification and systematic analysis of lncRNA-mRNA co-expression profiles in patients with cutaneous basal cell carcinoma
- The Contributions of Cancer-Testis and Developmental Genes to the Pathogenesis of Keratinocyte Carcinomas
- Twist1 as a Target for Prevention of Cutaneous Squamous Cell Carcinoma
- Immunohistochemical overexpression of TWIST1 in metastatic melanomas compared with primary melanomas and nevi
- Emerging biological functions of Twist1 in cell differentiation
- The Clinical Relevance of Epithelial-to-Mesenchymal Transition Hallmarks: A Cut-Off-Based Approach in Healthy and Cancerous Cell Lines
- Immunohistochemical overexpression of TWIST1 in metastatic melanomas compared with primary melanomas and nevi
- MiR-33a-5p suppresses progression inhibits the growth and metastasis of melanoma cells by targeting SNAI2
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