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EVI 1  (ecotropic viral integration site 1) is one of the most aggressive oncogenes associated with myeloid leukemia. We investigated  DNA  copy number aberrations in human hepatocellular carcinoma ( HCC ) cell lines using a high‐density oligonucleotide microarray. We found that a novel amplification at the chromosomal region 3q26 occurs in the  HCC  cell line  JHH ‐1, and that   MECOM   (  MDS 1  and   EVI 1  complex locus), which lies within the 3q26 region, was amplified. Quantitative  PCR  analysis of the three transcripts transcribed from   MECOM   indicated that only   EVI 1 , but not the fusion transcript   MDS 1– EVI 1  or   MDS 1 , was overexpressed in  JHH ‐1 cells and was significantly upregulated in 22 (61%) of 36 primary  HCC  tumors when compared with their non‐tumorous counterparts. A copy number gain of   EVI 1  was observed in 24 (36%) of 66 primary  HCC  tumors. High   EVI 1  expression was significantly associated with larger tumor size and higher level of des‐γ‐carboxy prothrombin, a tumor marker for  HCC . Knockdown of   EVI 1  resulted in increased induction of the cyclin‐dependent kinase inhibitor p15  INK   4B  by transforming growth factor ( TGF )‐β and decreased expression of c‐Myc, cyclin D1, and phosphorylated Rb in  TGF ‐β‐treated cells. Consequently, knockdown of   EVI 1  led to reduced  DNA  synthesis and cell viability. Collectively, our results suggest that   EVI 1  is a probable target gene that acts as a driving force for the amplification at 3q26 in  HCC  and that the oncoprotein  EVI 1 antagonizes  TGF ‐β‐mediated growth inhibition of  HCC  cells.

EVI 1 , a target gene for amplification at 3q26, antagonizes transforming growth factor‐β‐mediated growth inhibition in hepatocellular carcinoma