BACKGROUND: ZER6 is a C2H2 zinc finger transcription factor with two isoforms (p52-ZER6 and p71-ZER6), which are differentially repressed by a ligand-dependent interaction with estrogen receptor-alpha (ERalpha). We sought to determine if ZER6 proteins are expressed in ERalpha-positive breast cancer cells and if ZER6 is expressed in association with ERalpha in breast cancers. METHODS: The expression of ZER6 protein was examined by Western blot and the pattern of ZER6 expression was examined in a panel of ERalpha-positive and ERalpha-negative breast cancers using RT-PCR. RESULTS: COS-1 cells transfected with expression vectors for p52-ZER6 express a major protein of 52 kDa and a minor protein of 75 kDa, whereas cells transfected with the p71-ZER6 expression vector express a major protein of 77 kDa and a minor protein of 100 kDa. Breast carcinoma cells express ZER6-specific proteins of similar size, and expression of the p52-ZER6 isoform was only detected in the ERalpha-positive cell lines. In primary breast cancer tissue, 8/16 (50%) of the ERalpha-positive tumors had high ZER6 expression, whereas only 1/12 (8%) of the ERalpha-negative tumors had a high ZER6 level of expression. The relative abundance of ZER6 mRNA in the ERalpha-positive group was statistically greater than the ERalpha-negative group (188 versus 106, P < 0.05). CONCLUSIONS: We have confirmed that breast carcinoma cells express ZER6 proteins and identified an association between the level of ZER6 expression and ERalpha expression in primary breast cancers. These data support a role for the ZER6 transcription factors in regulating the expression of genes in hormone-responsive breast cancer.
BACKGROUND: ZER6 is a C2H2 zinc finger transcription factor with two isoforms (p52-ZER6 and p71-ZER6), which are differentially repressed by a ligand-dependent interaction with estrogen receptor-alpha (ERalpha). We sought to determine if ZER6 proteins are expressed in ERalpha-positive breast cancer cells and if ZER6 is expressed in association with ERalpha in breast cancers. METHODS: The expression of ZER6 protein was examined by Western blot and the pattern of ZER6 expression was examined in a panel of ERalpha-positive and ERalpha-negative breast cancers using RT-PCR. RESULTS: COS-1 cells transfected with expression vectors for p52-ZER6 express a major protein of 52 kDa and a minor protein of 75 kDa, whereas cells transfected with the p71-ZER6 expression vector express a major protein of 77 kDa and a minor protein of 100 kDa. Breast carcinoma cells express ZER6-specific proteins of similar size, and expression of the p52-ZER6 isoform was only detected in the ERalpha-positive cell lines. In primary breast cancer tissue, 8/16 (50%) of the ERalpha-positive tumors had high ZER6 expression, whereas only 1/12 (8%) of the ERalpha-negative tumors had a high ZER6 level of expression. The relative abundance of ZER6 mRNA in the ERalpha-positive group was statistically greater than the ERalpha-negative group (188 versus 106, P < 0.05). CONCLUSIONS: We have confirmed that breast carcinoma cells express ZER6 proteins and identified an association between the level of ZER6 expression and ERalpha expression in primary breast cancers. These data support a role for the ZER6 transcription factors in regulating the expression of genes in hormone-responsive breast cancer.