Myc down-regulation induces apoptosis in M14 melanoma cells by increasing p27(kip1) levels (Articolo in rivista)

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  • Myc down-regulation induces apoptosis in M14 melanoma cells by increasing p27(kip1) levels (Articolo in rivista) (literal)
Anno
  • 2001-01-01T00:00:00+01:00 (literal)
Alternative label
  • D'Agnano I. 1, Valentini A. 2, Fornari C. 3, Bucci B. 4, Starace G. 5, Felsani A. 6, Citro G. 7 (2001)
    Myc down-regulation induces apoptosis in M14 melanoma cells by increasing p27(kip1) levels
    in Oncogene (Basingstoke)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • D'Agnano I. 1, Valentini A. 2, Fornari C. 3, Bucci B. 4, Starace G. 5, Felsani A. 6, Citro G. 7 (literal)
Pagina inizio
  • 2814 (literal)
Pagina fine
  • 2825 (literal)
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  • Impact Factor 2002: 5.979 (literal)
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  • 20 (literal)
Rivista
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  • Anche la Dr.ssa Igea D'Agnano è personale CNR, attualmente all'Istituto Tecnologie Avanzate di Milano (literal)
Note
  • ISI Web of Science (WOS) (literal)
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  • 1,2,3,4,5,6 CNR-INNM, 7 Istituto Regina Elena (literal)
Titolo
  • Myc down-regulation induces apoptosis in M14 melanoma cells by increasing p27(kip1) levels (literal)
Abstract
  • In recent years, increasing evidence indicated the importance of a deregulated c-myc gene in the melanoma pathogenesis. We have previously demonstrated that treatment of melanoma cells with c-myc antisense oligodeoxynucleotides can inhibit cell proliferation and activate apoptosis. To gain insight into the mechanisms activated by Myc down-regulation, we have now developed an experimental model that allows modulating Myc protein expression in melanoma cells. This was achieved by originating stable melanoma cell clones expressing ecdysone-inducible c-myc antisense RNA. We show that the induction of c-myc antisense RNA in M14 melanoma cells leads to an inhibition of cell proliferation characterized by accumulation of cells in the G(1) phase of the cell cycle (up to 80%) and activation of apoptosis (50%). These data are associated with an increase of p27(kip1) levels and a significant reduction of the cdk2-associated kinase activity. In addition, we show that an ectopic overexpression of p27(kip1) in this experimental model can enhance the apoptotic rate. Our results indicate that down-regulation of Myc protein induces a G(1) arrest and activates apoptosis by increasing p27(kip1) content in melanoma cells, that are known to be defective for the p16-cyclinD/cdk4-pRb G(1) checkpoint. This is particularly relevant for identifying new therapeutic strategies based on the re-establishment of the apoptotic pathways in cancer cells (literal)
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