http://www.cnr.it/ontology/cnr/individuo/prodotto/ID4479
The role of PLZF in melanoma progression. (Articolo in rivista)
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- Label
- The role of PLZF in melanoma progression. (Articolo in rivista) (literal)
- Anno
- 2004-01-01T00:00:00+01:00 (literal)
- Alternative label
(1) Felicetti F, (1) Bottero L, (1) Felli N, (1) Mattia G, (1)Labbaye C, (2) Alvino E, (1) Peschle C, (3)Colombo MP, (1) Care' A. (2004)
The role of PLZF in melanoma progression.
in Oncogene (Basingstoke)
(literal)
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- (1) Felicetti F, (1) Bottero L, (1) Felli N, (1) Mattia G, (1)Labbaye C, (2) Alvino E, (1) Peschle C, (3)Colombo MP, (1) Care' A. (literal)
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Citations = 33 in Web of knoledge
Citations = 30 in Scopus (literal)
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- ISI Web of Science (WOS) (literal)
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- (1)Department of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanita`, 00161 Rome, Italy;
(2)Institute of Neurobiology and Molecular Medicine, CNR, 00100 Rome, Italy;
(3)Department of Experimental Oncology, Immunotherapy and GeneTherapy Unit, Istituto Nazionale Tumori, Milan, Italy (literal)
- Titolo
- The role of PLZF in melanoma progression. (literal)
- Abstract
- The promyelocytic leukemia zinc finger (PLZF) protein
has been described as a transcriptional repressor of
homeobox (HOX)-containing genes during embryogenesis.
As we previously demonstrated a functional link
between overexpression of HOXB7 and melanoma
progression, we investigated the lack of PLZF as the
possible cause of HOXB7 constitutive activation in these
neoplastic cells. Accordingly, we found PLZF expression
in melanocytes, but not in melanoma cells, a pattern
inversely related to that of HOXB7. PLZF retroviral gene
transduction was then performed in a panel of melanoma
cell lines, and tumorigenicity was compared with that of
empty vector-transduced control cell lines. Evaluation of
in vitro migration, invasion and adhesion indicated that
PLZF gene transduction induced a less malignant
phenotype, as confirmed through in vivo studies performed
in athymic nude mice. This reduced tumorigenicity was
not coupled with HOXB7 repression. In order to find more
about the molecular targets of PLZF, the gene expression
profiles of PLZF- and empty vector-transduced A375
melanoma cells were analysed by Atlas Cancer macroarray.
Among several genes modulated by PLZF enforced
expression, of particular interest were integrin avb3,
osteonectin/SPARC and matrix metalloprotease-9 that
were downmodulated, and the tyrosinase-related protein-1
that was upregulated in all the analysed samples. This
profile confirms the reduced tumorigenic phenotype with
reversion to a more differentiated, melanocyte like,
pattern, thus suggesting a suppressor role for PLZF in
solid tumors. Moreover, these results indicate that PLZF
and HOXB7 are functionally independent and that their
coupled deregulation may account for most of the
alterations described in melanomas. (literal)
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