Identification of ERF-1 as a member of the AP2 transcription factor family

McPherson, Lisa; Baichwal, Vijay; Weigel, Ronald J.

doi:10.1073/pnas.94.9.4342

Cited by 130 publications

(97 citation statements)

References 18 publications

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“…Table 3, the differential level of expression observed by the Atlas assay has been confirmed for some other genes by semiquantitative RT-PCR; in particular, a decreased expression has been confirmed for Sky tyrosine kinase receptor (Ohashi et al, 1994) and Erf-1 transcription factor (McPherson et al, 1997). On the contrary, RAD21, a factor involved in DNA repair and apoptotic cell death (Pati et al, 2002), and the anonymous cDNA KIAA0022 (Nomura et al, 1994) resulted in upregulation (not shown).…”

Section: Expression Of Plzf-regulated Genesmentioning

confidence: 78%

Role of PLZF in melanoma progression

et al. 2004

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The promyelocytic leukemia zinc finger (PLZF) protein has been described as a transcriptional repressor of homeobox (HOX)-containing genes during embryogenesis. As we previously demonstrated a functional link between overexpression of HOXB7 and melanoma progression, we investigated the lack of PLZF as the possible cause of HOXB7 constitutive activation in these neoplastic cells. Accordingly, we found PLZF expression in melanocytes, but not in melanoma cells, a pattern inversely related to that of HOXB7. PLZF retroviral gene transduction was then performed in a panel of melanoma cell lines, and tumorigenicity was compared with that of empty vector-transduced control cell lines. Evaluation of in vitro migration, invasion and adhesion indicated that PLZF gene transduction induced a less malignant phenotype, as confirmed through in vivo studies performed in athymic nude mice. This reduced tumorigenicity was not coupled with HOXB7 repression. In order to find more about the molecular targets of PLZF, the gene expression profiles of PLZF-and empty vector-transduced A375 melanoma cells were analysed by Atlas Cancer macroarray. Among several genes modulated by PLZF enforced expression, of particular interest were integrin avb3, osteonectin/SPARC and matrix metalloprotease-9 that were downmodulated, and the tyrosinase-related protein-1 that was upregulated in all the analysed samples. This profile confirms the reduced tumorigenic phenotype with reversion to a more differentiated, melanocyte like, pattern, thus suggesting a suppressor role for PLZF in solid tumors. Moreover, these results indicate that PLZF and HOXB7 are functionally independent and that their coupled deregulation may account for most of the alterations described in melanomas.

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Section: Expression Of Plzf-regulated Genesmentioning

confidence: 78%

Role of PLZF in melanoma progression

et al. 2004

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“…6 The estrogen receptor gene had previously been shown to be controlled by AP-2. 17 These results, however, were questioned by a different study, which found AP-2 expression to be higher in normal breast epithelia than in invasive tumors, 18 confirming a previous study, which had suggested that AP-2 might represent a novel tumor-suppressor gene because AP-2alpha/beta inversely correlated with ErbB-2 in invasive breast carcinoma. 19 To our knowledge, none of the studies addressed the spatial expression patterns of the different AP-2 isoforms on either normal breast tissue or breast tumor specimens.…”

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confidence: 69%

Distinct spatial expression patterns of AP-2alpha and AP-2gamma in non-neoplastic human breast and breast cancer

et al. 2005

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Although transcription factors AP-2alpha and AP-2gamma have been implicated in the control of estrogen receptor (ER) and ErbB-2, their impact for breast cancer is still controversial. To better understand the role of AP-2 proteins in mammary neoplasia, the analysis of their spatial expression pattern in normal breast and breast cancer is required. A total of 51 specimens of female breast cancer patients and a tissue microarray containing 93 additional female breast cancer cases were immunohistochemically stained for AP-2alpha, AP2gamma, ER and ErbB-2. In 70 cases of the tissue microarray, survival data comprising a period of up to 30 years were present. In non-neoplastic breast tissue, AP-2alpha was expressed in the inner glandular cell layer while AP-2gamma was expressed in the outer myoepithelial cell layer. Ductal carcinoma in situ revealed strongly AP-2alpha-positive tumor cells surrounded by a layer of AP-2gamma-positive myoepithelial cells. In invasive carcinoma, expression of AP-2alpha and AP-2gamma was variable. High expression of ER and AP2alpha showed better survival rates than low expression of these markers. AP-2gamma expression had no effect on survival. These results for the first time reveal a distinct spatial expression pattern of AP-2alpha and AP-2gamma in normal breast and in ductal carcinoma in situ with specific AP-2gamma expression in myoepithelium. High ER and AP-2alpha expression in invasive breast cancer showed favorable survival rates. Therefore, AP-2alpha expression seems to be associated with better prognosis of breast cancer. AP-2gamma expression has no influence on survival reflecting that myoepithelial cells are not involved in the neoplastic process.

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“…Methylation outside of the consensus sequence for SP1 induced a significant decrease in SP1 binding, leading to a reduced target gene expression (Zhu et al, 2003). AP-2 regulates genes involved in various biological functions, including p21 WAF/CIP (Zeng et al, 1997), transforming growth factor-a (Wang et al, 1997), estrogen receptor (McPherson et al, 1997), and tyrosine kinase receptor gene c-KIT (Huang et al, 1998). AP-2 also negatively regulates a number of genes, including c-myc (Gaubatz et al, 1995) and c-/EBP-a (Jiang et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Hypomethylation of WNT5A, CRIP1 and S100P in prostate cancer

et al. 2007

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Oligoarray analysis of a matched pair of prostate cancer and normal cell lines derived from the same radical prostatectomy specimen identified 113 candidate hypomethylated genes that were overexpressed in the cancer cells and contained CpG islands. Hypomethylation of wingless-related MMTV integration site 5A (WNT5A), S100 calcium-binding protein P (S100P) and cysteine-rich protein 1(CRIP1) was confirmed in the cancer cells by bisulfite sequencing. Treatment of the corresponding normal prostate epithelial cells 1542-NPTX with the DNA methyltransferase inhibitor 5-Aza-2 0 -deoxycytidine (5-aza-CdR) induced higher levels of mRNA expression and partial loss of methylation on these genes. Primary prostate cancers were tested using methylation-specific polymerase chain reaction. WNT5A was hypomethylated in 11/17 (65%) tumors, S100P in 8/16 (50%) and CRIP1 in 13/20 (65%). Bisulfite sequencing of a section of the 5 0 untranslated region (UTR) of WNT5A revealed that three CpG sites (15, 24 and 35) were consistently methylated (93%) in the normal cell line and normal tissues, but not in the prostate cancer cell line and eight primary prostate cancers. Multiple putative binding sites for the transcription factors SP1 and AP-2 were found adjacent to CpG sites 15 and 24. A putative c-Myb binding site was located within the CpG site 35. Anti-c-Myb antibody co-precipitation with WNT5A was methylation-sensitive in 1542-NPTX cells. It is likely that an epigenetic mechanism regulates WNT5A expression in prostate cancer.

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Identification of ERF-1 as a member of the AP2 transcription factor family

Cited by 130 publications

References 18 publications

Role of PLZF in melanoma progression

Role of PLZF in melanoma progression

Distinct spatial expression patterns of AP-2alpha and AP-2gamma in non-neoplastic human breast and breast cancer

Hypomethylation of WNT5A, CRIP1 and S100P in prostate cancer

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