Changes in the Expression of Many Ets Family Transcription Factors and of Potential Target Genes in Normal Mammary Tissue and Tumors

Galang, Christina K.; Muller, William J.; Foos, Gabriele; Oshima, Robert G.; Hauser, Craig A.

doi:10.1074/jbc.m311887200

Cited by 125 publications

(113 citation statements)

References 63 publications

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“…Following affinity purification, the antibody was tested for specificity by Western blot assay and by immunohistochemical staining of cells from MCF-7 breast tumor cell line and from tissue sections from primary breast and prostate tumors. The data are shown in (11) and of Pse (prostate specific Ets, the mouse homologue of PDEF) mRNA (17). These results together show the specificity of the anti-PDEF antibody as well as its suitability for use in immunohistochemical analysis of PDEF expression in primary tumors.…”

Section: Anti-pdef Antibody Shows Specific Reactivity With Pdefmentioning

confidence: 70%

“…Alternatively, since the anti-PDEF antibodies used in two of the three previous studies (19,20) were generated against the full-length PDEF protein, they carried the potential for crossreaction with other Ets factors in the immunohistochemical assay. The latter potential stems from: i) the high degree of sequence homology approaching 45 to 55% amino acid sequence identity in the DNA binding domain between PDEF and other Ets factors (11); and ii) the large number of Ets factors that are expressed in normal mammary gland, and several at much higher levels than Pse or PDEF (17,22). The third study (21) used antibody raised against the same N-terminal segment of PDEF as used in this study, however, the specificity of the immunohistochemical assay for PDEF was not demonstrated in that study.…”

Section: Discussionmentioning

confidence: 99%

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Expression characteristics of prostate-derived Ets factor support a role in breast and prostate cancer progression

et al. 2007

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The purpose of this study was to understand the characteristics of PDEF protein expression in breast and prostate cancer progression. A polyclonal antibody specific to PDEF was raised and reacted with tissue microarrays consisting of benign breast, in situ ductal, invasive ductal and invasive lobular breast carcinomas. The antibody was also reacted with tissue microarrays including benign prostate, prostate intra-epithelial neoplasias and prostate carcinomas. Increased expression of PDEF was identified in 18%, 50%, 46% and 51% of benign breast tissues, intraductal, invasive ductal and invasive lobular carcinomas, respectively. Importantly, in matched samples of benign breast versus tumor, 90% showed higher expression of PDEF in the tumor tissue. Moreover, in invasive breast carcinomas, increased PDEF expression tended to correlate with Her2/neu over expression. Increased expression of PDEF was also found in 27%, 33% and 40% of benign prostate tissues, PIN samples and prostate adenocarcinomas, respectively. Again, in matching samples of cancer versus benign and cancer versus PIN, 68% and 70% respectively showed increased expression in the malignant tissue. Moreover, PDEF was found to be more highly expressed in tumors with intermediate or high Gleason score compared to low grade tumors (P<0.01). Additionally, R1881 treatment induced PDEF expression in the LNCaP prostate tumor cell line, suggesting regulation of PDEF by androgens in vivo. Together, these results for the first time show frequent increased expression of PDEF protein in breast and prostate tumors and support a role for PDEF in breast and prostate cancer progression.

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Section: Anti-pdef Antibody Shows Specific Reactivity With Pdefmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 99%

Expression characteristics of prostate-derived Ets factor support a role in breast and prostate cancer progression

et al. 2007

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“…In pathological processes, the presence of ERM mRNA has been associated with breast cancer metastasis. High levels of this messenger are detected in human and mouse (Galang et al, 2004) metastatic mammary cancer cells. In vivo, in mouse mammary tumors producing high levels of ERM mRNA, ectopic expression of a dominant-negative Ets mutant increases the mouse survival rate (Shepherd et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

The 26S proteasome system degrades the ERM transcription factor and regulates its transcription-enhancing activity

et al. 2006

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ERM is a member of the ETS transcription factor family. High levels of the corresponding mRNA are detected in a variety of human breast cancer cell lines, as well as in aggressive human breast tumors. As ERM protein is almost undetectable in these cells, high degradation of this transcription factor has been postulated. Here we have investigated whether ERM degradation might depend on the proteasome pathway. We show that endogenous and ectopically expressed ERM protein is short-lived protein and undergoes proteasome-dependent degradation. Deletion mutagenesis studies indicate that the 61 C-terminal amino acids of ERM are critical for its proteolysis and serve as a degradation signal. Although ERM conjugates with ubiquitin, this post-translational modification does not depend on the C-terminal domain. We have used an Ets-responsive ICAM-1 reporter plasmid to show that the ubiquitin-proteasome pathway can affect transcriptional function of ERM. Thus, ERM is subject to degradation via the 26S proteasome pathway, and this pathway probably plays an important role in regulating ERM transcriptional activity.

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“…Recently, Ese-2, a member of the ESE subfamily of Ets factors, has been recognized as an asthma candidate gene [24], and its expression is correlated with that of the gene encoding maspin, a tumor suppressor protein [25]. Little is known, however, about the role of Ese-2 in gene regulation.…”

Section: Introductionmentioning

confidence: 99%

Epithelium-specific ets transcription factor 2 upregulates cytokeratin 18 expression in pulmonary epithelial cells through an interaction with cytokeratin 18 intron 1

YANIW,

2005

Cell Res

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The role of Ese-2, an Ets family transcription factor, in gene regulation is not known. In this study, the interaction between Ese-2 and cytokeratin 18 (K18) intron 1 was characterized in lung epithelial cells. Reporter gene assays showed Ese-2 was able to upregulate K18 intron 1 enhanced reporter gene expression by approximately 2-fold. We found that full length Ese-2 did not bind DNA strongly, therefore truncated versions of the protein, containing the ETS domain or Pointed domain, were created and tested in electrophoresis mobility shift assays. Multiple interactions between the ETS domain and putative DNA binding sites within K18 intron 1 were observed, which led to the determination of a possible Ese-2 DNA binding consensus sequence. These experiments suggest that Ese-2 could play a role in the regulation of K18 expression in lung epithelial cells.

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Changes in the Expression of Many Ets Family Transcription Factors and of Potential Target Genes in Normal Mammary Tissue and Tumors

Cited by 125 publications

References 63 publications

Expression characteristics of prostate-derived Ets factor support a role in breast and prostate cancer progression

Expression characteristics of prostate-derived Ets factor support a role in breast and prostate cancer progression

The 26S proteasome system degrades the ERM transcription factor and regulates its transcription-enhancing activity

Epithelium-specific ets transcription factor 2 upregulates cytokeratin 18 expression in pulmonary epithelial cells through an interaction with cytokeratin 18 intron 1

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