Poorly differentiated squamous cell carcinomas of the skin can express vimentin

Iyer, P. V. Krishna; Leong, Anthony S.‐Y.

doi:10.1111/j.1600-0560.1992.tb01556.x

Cited by 30 publications

(13 citation statements)

References 21 publications

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“…Consequently, epithelial polarity declined showing irregular clusters of proliferating and differentiating cells. As hallmark, seen in skin squamous cell carcinomas [173], nonepidermal “simple” keratins K8/K18 and vimentin (an indicator for epithelial-mesenchymal transition/EMT) appeared at the invading front [171]. The areas of proliferation, expanding suprabasally, were strongly decorated by β 1-integrins and α 6 β 4 [64], similar to changes observed in mouse models of two-stage carcinogenesis ([63]; references in [174]).…”

Section: Human Cells Rebuild Epidermal Architecture In Mouse Xenogmentioning

confidence: 99%

Skin Basement Membrane: The Foundation of Epidermal Integrity—BM Functions and Diverse Roles of Bridging Molecules Nidogen and Perlecan

Breitkreutz

Koxholt

Thiemann

et al. 2013

BioMed Research International

180

132

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The epidermis functions in skin as first defense line or barrier against environmental impacts, resting on extracellular matrix (ECM) of the dermis underneath. Both compartments are connected by the basement membrane (BM), composed of a set of distinct glycoproteins and proteoglycans. Herein we are reviewing molecular aspects of BM structure, composition, and function regarding not only (i) the dermoepidermal interface but also (ii) the resident microvasculature, primarily focusing on the per se nonscaffold forming components perlecan and nidogen-1 and nidogen-2. Depletion or functional deficiencies of any BM component are lethal at some stage of development or around birth, though BM defects vary between organs and tissues. Lethality problems were overcome by developmental stage- and skin-specific gene targeting or by cell grafting and organotypic (3D) cocultures of normal or defective cells, which allows recapitulating BM formation de novo. Thus, evidence is accumulating that BM assembly and turnover rely on mechanical properties and composition of the adjacent ECM and the dynamics of molecular assembly, including further “minor” local components, nidogens largely functioning as catalysts or molecular adaptors and perlecan as bridging stabilizer. Collectively, orchestration of BM assembly, remodeling, and the role of individual players herein are determined by the developmental, tissue-specific, or functional context.

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Section: Human Cells Rebuild Epidermal Architecture In Mouse Xenogmentioning

confidence: 99%

Skin Basement Membrane: The Foundation of Epidermal Integrity—BM Functions and Diverse Roles of Bridging Molecules Nidogen and Perlecan

Breitkreutz

Koxholt

Thiemann

et al. 2013

BioMed Research International

180

132

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“…Vimentin is an intermediate filament found predominantly in mesenchymal cells, but not in epithelial cells. However, it also exists in some carcinoma cell lines [4-6] and squamous cell carcinomas [7,8]. …”

Section: Introductionmentioning

confidence: 99%

Study of β-catenin, E-cadherin and vimentin in oral squamous cell carcinoma with and without lymph node metastases

et al. 2014

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BackgroundDespite great improvement in the surgical treatment and adjunctive therapy for oral squamous cell carcinoma (OSCC), prognosis remains dismal in advanced cases. Regional metastatic disease is known to reduce recurrence free survival and disease specific survival significantly. The present study was conducted to evaluate the role of cell adhesion molecules β-catenin, E-cadherin and vimentin in predicting tumour metastasis of OSCC.MethodsA total of sixty cases of oral squamous cell carcinoma were included for the study which comprised of 30 cases with lymph node metastases and 30 cases without metastases. Immunohistochemistry was performed for β-catenin, E-cadherin and vimentin on both the test groups along with 30 controls from normal buccal mucosa and inflammatory lesions each.ResultsThere was no significant difference between the immunoreactivity for β-catenin, E-cadherin and vimentin between OSCC with and without lymph node metastases. Vimentin immunopositivity was noted with varying intensity in all cases of OSCC.ConclusionsE-cadherin and β-catenin are probably not the key determinants for regional metastases in OSCC. The role of vimentin expression in OSCC and metastases is controversial and needs to be studied further.Virtual slidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/6506095201182002.

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“…Certain poorly differentiated carcinomas have been found to lose desmosomes and adherens junctions, express vimentin, acquire a spindle cell phenotype, overexpress proteases, and become highly motile; these changes are associated with enhanced invasive and metastatic potential. 1,[3][4][5][6] Dysregulation of genes important in developmental EMT has been implicated in these EMT-like processes. 7 Two highly conserved members of the Snail family of zinc-finger transcription factors, Snai1 (Snail) and Snai2 (Slug), play roles in developmental EMT.…”

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confidence: 99%

Snai2 Expression Enhances Ultraviolet Radiation-Induced Skin Carcinogenesis

Newkirk

Parent

Fossey

et al. 2007

The American Journal of Pathology

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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. (Am J Pathol

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Poorly differentiated squamous cell carcinomas of the skin can express vimentin

Cited by 30 publications

References 21 publications

Skin Basement Membrane: The Foundation of Epidermal Integrity—BM Functions and Diverse Roles of Bridging Molecules Nidogen and Perlecan

Skin Basement Membrane: The Foundation of Epidermal Integrity—BM Functions and Diverse Roles of Bridging Molecules Nidogen and Perlecan

Study of β-catenin, E-cadherin and vimentin in oral squamous cell carcinoma with and without lymph node metastases

Snai2 Expression Enhances Ultraviolet Radiation-Induced Skin Carcinogenesis

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