Kuphal S, Schneider N, Massoumi R, Hellerbrand C, Boßerhoff AK (2017)
Publication Type: Journal article
Publication year: 2017
Book Volume: 14
Pages Range: 7262-7268
Journal Issue: 6
DOI: 10.3892/ol.2017.7120
CYLD lysine 63 deubiquitinase (CYLD) was originally identified as a tumor suppressor that is mutated in familial cylindromatosis. Unlike in cylindromatosis, downregulation of the deubiquitinase CYLD in melanoma, a highly aggressive tumor, is not caused by mutations in the CYLD gene, but rather by a constitutive and high expression of the snail family transcriptional repressor 1 (SNAIL1). A reduced CYLD level leads to B-cell lymphoma-3/p50/p52-dependent nuclear factor-κB activation, which in turn triggers the expression of genes such as cyclin D1 and N-cadherin. Elevated levels of cyclin D1 and N-cadherin promote melanoma proliferation and invasion. By analyzing the regulation of CYLD expression in melanocytes, the present study identified a signaling pathway that is regulated in response to ultraviolet B (UVB) radiation in melanocytes. UVB light leads to an extracellular signal-regulated kinase-mediated induction of SNAIL1 and subsequent downregulation of CYLD expression in normal human epithelial melanocytes. The UVB-mediated suppression of CYLD in melanocytes may have a key role in the reaction to UV stimuli, and may also potentially be involved in the early malignant transformation processes.
APA:
Kuphal, S., Schneider, N., Massoumi, R., Hellerbrand, C., & Boßerhoff, A.K. (2017). UVB radiation represses CYLD expression in melanocytes. Oncology Letters, 14(6), 7262-7268. https://dx.doi.org/10.3892/ol.2017.7120
MLA:
Kuphal, Silke, et al. "UVB radiation represses CYLD expression in melanocytes." Oncology Letters 14.6 (2017): 7262-7268.
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