An ATF2-derived peptide sensitizes melanomas to apoptosis and inhibits their growth and metastasis

Anindita Bhoumik, Tian Gui Huang, Vladimir Ivanov, Lisa Gangi, Rui F. Qiao, Savio L.C. Woo, Shu Hsia Chen, ZE'Ev Ronai

Research output: Contribution to journalArticle

73 Scopus citations

Abstract

Melanomas are among the aggressive tumor types because of their notorious resistance to treatment and their high capacity to metastasize. ATF2 is among transcription factors implicated in the progression of melanoma and its resistance to treatment. Here we demonstrate that the expression of a peptide spanning amino acids 50-100 of ATF2 (ATF250-100) reduces ATF2 transcriptional activities while increasing the expression and activity of c-Jun. Altering the balance of Jun/ATF2 transcriptional activities sensitized melanoma cells to apoptosis, an effect that could be attenuated by inhibiting c-Jun. Inhibition of ATF2 via RNA interference likewise increased c-Jun expression and primed melanoma cells to undergo apoptosis. Growth and metastasis of SW1 and B16F10 mouse melanomas were inhibited by ATF250-100 to varying degrees up to a complete regression, depending on the mode (inducible, constitutive, or adenoviral delivery) of its expression. Thus, by attenuating ATF2 and inducing c-Jun activity, ATF250-100 inhibits melanoma growth and metastasis.

Original languageEnglish (US)
Pages (from-to)643-650
Number of pages8
JournalJournal of Clinical Investigation
Volume110
Issue number5
DOIs
StatePublished - Sep 2002

ASJC Scopus subject areas

  • Medicine(all)

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