EVI1, a target gene for amplification at 3q26, antagonizes transforming growth factor-β-mediated growth inhibition in hepatocellular carcinoma.
作者： Kohichiroh Yasui , Chika Konishi , Yasuyuki Gen , Mio Endo , Osamu Dohi
DOI: 10.1111/CAS.12694
关键词:
摘要: EVI1 (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. found that novel amplification at chromosomal region 3q26 occurs HCC line JHH-1, and MECOM (MDS1 complex locus), which lies within region, was amplified. Quantitative PCR analysis three transcripts transcribed from indicated only EVI1, but not fusion transcript MDS1–EVI1 or MDS1, overexpressed JHH-1 cells significantly upregulated 22 (61%) 36 primary tumors when compared their non-tumorous counterparts. A copy gain observed 24 (36%) 66 tumors. High expression larger tumor size higher level des-γ-carboxy prothrombin, marker for HCC. Knockdown resulted increased induction cyclin-dependent kinase inhibitor p15INK4B by transforming growth factor (TGF)-β decreased c-Myc, cyclin D1, phosphorylated Rb TGF-β-treated cells. Consequently, knockdown led to reduced synthesis viability. Collectively, our results suggest probable target gene acts as driving force oncoprotein antagonizes TGF-β-mediated inhibition
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