AIM: To determine whether JUN (the oncogene encoding c-Jun protein) is amplified and overexpressed in hepatocellular carcinoma (HCC). MATERIALS AND METHODS: DNA copy number aberrations were investigated using a high-density oligonucleotide microarray. DNA copy numbers were determined by fluorescence in situ hybridization. Genomic DNA and mRNA were quantified using real-time quantitative PCR. RESULTS: A novel amplification was found at the chromosomal region 1p32-31 in a JHH-2 HCC cell line within which JUN is amplified and overexpressed. However, no copy number gain of JUN (>2-fold) was observed in 34 primary HCC tumors. Rather, a loss of JUN (<0.5-fold) was seen in 13 (38%) out of the 34 tumors and expression of JUN was significantly lower in 26 (70%) out of the 37 HCC tumors compared with their nontumorous counterparts. CONCLUSION: Although JUN was amplified and overexpressed in JHH-2 HCC cells, amplification and overexpression of JUN may be rare in primary HCCs.
AIM: To determine whether JUN (the oncogene encoding c-Jun protein) is amplified and overexpressed in hepatocellular carcinoma (HCC). MATERIALS AND METHODS: DNA copy number aberrations were investigated using a high-density oligonucleotide microarray. DNA copy numbers were determined by fluorescence in situ hybridization. Genomic DNA and mRNA were quantified using real-time quantitative PCR. RESULTS: A novel amplification was found at the chromosomal region 1p32-31 in a JHH-2 HCC cell line within which JUN is amplified and overexpressed. However, no copy number gain of JUN (>2-fold) was observed in 34 primary HCC tumors. Rather, a loss of JUN (<0.5-fold) was seen in 13 (38%) out of the 34 tumors and expression of JUN was significantly lower in 26 (70%) out of the 37 HCC tumors compared with their nontumorous counterparts. CONCLUSION: Although JUN was amplified and overexpressed in JHH-2 HCC cells, amplification and overexpression of JUN may be rare in primary HCCs.