Abstract
Basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) are the most frequent tumors in the Caucasian population. The formation of these tumors is a consequence of long term UV-exposure of the skin. UV-light induces DNA damage in cells. If the damaged DNA cannot be repaired or the DNA damaged cell is not eliminated by apoptosis (so-called sunburn cells), cell transformation and tumor development can be the outcome. Fas-ligand (FasL), a member of the tumor necrosis superfamily, is a key molecule involved in the elimination of sunburn cells. FasL is expressed in normal skin epidermis, preferentially in the basal layer. Regulation of FasL expression has a dual effect on cancerogenesis. On the one hand, FasL expression is down regulated in skin epidermis by UV irradiation leading to the loss of its sensor function and thereby increasing the risk of cell transformation and skin tumor development. On the other hand, once BCC or SCC have developed, FasL is strongly up-regulated. High expression of FasL may now serve to protect the tumor from the attack of immune effector cells. To prove the immune escape hypothesis in vivo, the prevention or downregulation of FasL expression in tumor tissue is required. Two approaches were successfully applied to silence the FasL gene in BCC tissues ex vivo, the antisense technology and RNA interference with small interfering RNA duplexes. With both techniques FasL expression can be efficiently downregulated in BCC tissues pathing the way to test the immune escape hypothesis in vivo.
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© 2006 Landes Bioscience and Springer Science+Business Media
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Erb, P., Ji, J., Wernli, M., Büchner, S.A. (2006). Apoptosis and Cancerogenesis of Basal Cell and Squamous Cell Carcinoma. In: Molecular Mechanisms of Basal Cell and Squamous Cell Carcinomas. Medical Intelligence Unit. Springer, Boston, MA. https://doi.org/10.1007/0-387-35098-5_11
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DOI: https://doi.org/10.1007/0-387-35098-5_11
Publisher Name: Springer, Boston, MA
Print ISBN: 978-0-387-26046-4
Online ISBN: 978-0-387-35098-1
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