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Title: The activation of human endogenous retrovirus K (HERV-K) is implicated in melanoma cell malignant transformation

Journal Article · · Experimental Cell Research
 [1];  [2]; ;  [1];  [1];  [2];  [3];  [4]; ;  [1]
  1. Department of Experimental Medicine and Biochemical Science - University of Rome 'Tor Vergata', via Montpellier, 00133 - Rome (Italy)
  2. Institute of Neurobiology and Molecular Medicine - ARTOV, CNR via Fosso del Cavaliere 100, 00133 - Rome (Italy)
  3. Department of Life Sciences, University of Messina, Salita Sperone 31, 98166 - Messina (Italy)
  4. Istituto Superiore di Sanita, Viale Regina Elena, 299, 00161 - Rome (Italy)

Melanoma development is a multi-step process arising from a series of genetic and epigenetic events. Although the sequential stages involved in progression from melanocytes to malignant melanoma are clearly defined, our current understanding of the mechanisms leading to melanoma onset is still incomplete. Growing evidence show that the activation of endogenous retroviral sequences might be involved in transformation of melanocytes as well as in the increased ability of melanoma cells to escape immune surveillance. Here we show that human melanoma cells in vitro undergo a transition from adherent to a more malignant, non-adherent phenotype when exposed to stress conditions. Melanoma-derived non-adherent cells are characterized by an increased proliferative potential and a decreased expression of both HLA class I molecules and Melan-A/MART-1 antigen, similarly to highly malignant cells. These phenotypic and functional modifications are accompanied by the activation of human endogenous retrovirus K expression (HERV-K) and massive production of viral-like particles. Down-regulation of HERV-K expression by RNA interference prevents the transition from the adherent to the non-adherent growth phenotype in low serum. These results implicate HERV-K in at least some critical steps of melanoma progression.

OSTI ID:
21176185
Journal Information:
Experimental Cell Research, Vol. 315, Issue 5; Other Information: DOI: 10.1016/j.yexcr.2008.12.023; PII: S0014-4827(08)00547-8; Copyright (c) 2008 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0014-4827
Country of Publication:
United States
Language:
English