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Background  Analysis of chromosomal rearrangements within primary tumors has been influential in the identification of novel oncogenes. Identification of the “driver” gene(s) within cancer-derived amplicons is, however, hampered by the fact that most amplicons contain many gene products. Amplification of 1q21–1q23 is strongly associated with liposarcomas and microarray-based comparative genomic hybridization narrowed down the likely candidate oncogenes to two: the activating transcription factor 6 ( atf6 ) and the dual specificity phosphatase 12 ( dusp12 ). While  atf6  is an established transcriptional regulator of the unfolded protein response, the potential role of  dusp12  in cancer remains uncharacterized.    Methodology/Principal Findings  To evaluate the oncogenic potential of  dusp12 , we established stable cell lines that ectopically over-express  dusp12  in isolation and determined whether this cell line acquired properties frequently associated with transformed cells. Here, we demonstrate that cells over-expressing  dusp12  display increased cell motility and resistance to apoptosis. Additionally, over-expression of  dusp12  promoted increased expression of the  c-met  proto-oncogene and the collagen and laminin receptor intergrin alpha 1 ( itga1 ) which is implicated in metastasis.    Significance  Collectively, these results suggest that  dusp12  is oncologically relevant and exposes a potential association between  dusp12  and established oncogenes that could be therapeutically targeted.

Characterization of a Human Cell Line Stably Over-Expressing the Candidate Oncogene, Dual Specificity Phosphatase 12