z-logo
Premium
MEL4B3, a novel mRNA is induced in skin tumors and regulated by TGF‐β and pro‐inflammatory cytokines
Author(s) -
Anderegg Ulf,
Breitschwerdt Kerstin,
Köhler Martin J.,
Sticherling Michael,
Haustein UweFrithjof,
Simon Jan C.,
Saalbach Anja
Publication year - 2005
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.0906-6705.2005.00349.x
Subject(s) - melanoma , basal cell carcinoma , biology , cancer research , transforming growth factor , tumor necrosis factor alpha , cell culture , epidermis (zoology) , cytokine , pathology , cell , transforming growth factor beta , metastasis , immunology , medicine , microbiology and biotechnology , cancer , basal cell , anatomy , genetics
  Tumor–stroma interactions play a decisive role in the growth and metastasis of solid tumors, and involve signalling either by soluble mediators or direct cell–cell interaction. Here, we report the isolation and characterisation of a novel cDNA (MEL4B3), which is induced in cultured dermal fibroblasts exposed to supernatants of melanoma cell lines. MEL4B3 shares high homology with two predicted cDNA sequences for which no activity has so far been described. In situ hybridisation revealed the expression of MEL4B3 in malignant melanoma increasing with tumor depth; in basal cell carcinoma and in squamous cell carcinoma. MEL4B3 was barely detectable in normal skin or non‐malignant melanocytic naevi. Furthermore, MEL4B3 was expressed at high level in the epidermis of psoriatic skin. In vitro , the expression of MEL4B3 was found to be induced by the exposure of human dermal fibroblasts to melanoma cell culture supernatants or to transforming growth factor‐β, interleukin‐1 and tumor necrosis factor‐α. The expression MEL4B3 therefore reflects closely cell activation occurring during tumor growth, metastasis and inflammation.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here