A Transcriptionally Inactive ATF2 Variant Drives Melanomagenesis

Giuseppina Claps, Yann Cheli, Tongwu Zhang, Marzia Scortegagna, Eric Lau, Hyungsoo Kim, Jianfei Qi, Jian Liang Li, Brian James, Andreas Dzung, Mitchell P. Levesque, Reinhard Dummer, Nicholas K. Hayward, Marcus Bosenberg, Kevin M. Brown, Ze'ev A. Ronai

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


Melanoma is one of the most lethal cutaneous malignancies, characterized by chemoresistance and a striking propensity to metastasize. The transcription factor ATF2 elicits oncogenic activities in melanoma, and its inhibition attenuates melanoma development. Here, we show that expression of a transcriptionally inactive form of Atf2 (Atf2δ8,9) promotes development of melanoma in mouse models. Atf2δ8,9-driven tumors show enhanced pigmentation, immune infiltration, and metastatic propensity. Similar to mouse Atf2δ8,9, we have identified a transcriptionally inactive human ATF2 splice variant 5 (ATF2SV5) that enhances the growth and migration capacity of cultured melanoma cells and immortalized melanocytes. ATF2SV5 expression is elevated in human melanoma specimens and is associated with poor prognosis. These findings point to an oncogenic function for ATF2 in melanoma development that appears to be independent of its transcriptional activity.

Original languageEnglish
Pages (from-to)1884-1892
Number of pages9
JournalCell Reports
Issue number9
StatePublished - 31 May 2016
Externally publishedYes


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