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Publication : A Transcriptionally Inactive ATF2 Variant Drives Melanomagenesis.

First Author  Claps G Year  2016
Journal  Cell Rep Volume  15
Issue  9 Pages  1884-92
PubMed ID  27210757 Mgi Jnum  J:235959
Mgi Id  MGI:5804054 Doi  10.1016/j.celrep.2016.04.072
Citation  Claps G, et al. (2016) A Transcriptionally Inactive ATF2 Variant Drives Melanomagenesis. Cell Rep 15(9):1884-92
abstractText  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 (Atf2(Delta8,9)) promotes development of melanoma in mouse models. Atf2(Delta8,9)-driven tumors show enhanced pigmentation, immune infiltration, and metastatic propensity. Similar to mouse Atf2(Delta8,9), we have identified a transcriptionally inactive human ATF2 splice variant 5 (ATF2(SV5)) that enhances the growth and migration capacity of cultured melanoma cells and immortalized melanocytes. ATF2(SV5) 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.
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