Regulation of estrogen receptor and epidermal growth factor receptor by tamoxifen under high and low estrogen environments in MCF-7 cells grown in athymic mice.

Koibuchi, Yukio; Iino, Y; Uchida, Tsutomu; Andoh, Tatsumasa; Horii, Y; Nagasawa, Mitsuru; Horiguchi, Jun; Maemura, Michio; Takei, Hiroyuki; Yokoe, Takao; Morishita, Yasuo

doi:10.3892/or.7.1.135

Cited by 8 publications

(10 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Table shows that epidermal growth factor receptor (EGFR) is decreased 3-fold in the group receiving estrogen versus the group with the same tumor implant but not receiving estrogen and without tumor growth. This result is consistent with other observations on the levels of EGFR in athymic mice tumors (MCF-7) in the presence and absence of estrogen. , We also observed that macrophage colony-stimulating factor 1 receptor (CSF1R), a transmembrane kinase receptor, was also downregulated in the group of mice with growing tumors versus controls, which is consistent with previous studies. , Another example is alpha-1- antitrypsin, which was decreased in the estrogen-treated group (Table ) and levels of this protein are negatively correlated with growth of MCF-7 cells . Insulin receptor substrate 2 (IRS2) showed a 2-fold increase on estrogen treatment of the MCF-7 implanted athymic mice which is supported by the report of Lee et al In studies with athymic mice with MCF-7 tumors, it was found that tamoxifen is a tumorstatic agent .…”

Section: Resultssupporting

confidence: 93%

See 1 more Smart Citation

A Proteomic Analysis of the Plasma Glycoproteins of a MCF-7 Mouse Xenograft: A Model System for the Detection of Tumor Markers

et al. 2008

View full text Add to dashboard Cite

In this study, we report a plasma proteomic analysis of a mouse MCF7 xenograft, using a novel platform named M-LAC (multilectin affinity chromatography), in an attempt to identify putative serum biomarkers of tumor presence and response to therapy. The use of the M-LAC platform enabled us to focus on secreted proteins as well as remove interference from serum albumin and other nonglycosylated proteins. The study focused on the MCF7 human xenograft tumor model which enabled us to distinguish tumor proteins (human peptide sequences) from host-derived murine proteins, potentially discriminating tumor- versus supporting tissue-derived markers. A large set of murine proteins was identified in this study, including several signaling molecules such as EGFR, interleukin-6 receptor, protein-kinase C, and phosphatidylinositol kinase which changed in plasma levels relative to tumor-free animals. We also detected in the samples with maximal tumor growth a number of human tumor-derived proteins linked to cell signaling, immune response, and transcriptional regulation. This is the first report where tumor-derived peptides could be detected in the serum of a xenograft model. We conclude that the M-LAC approach may be used to detect plasma proteins of potential biological significance in tumor-bearing animals and warrants further study in terms of increasing the sensitivity of the method for the characterization of low level tumor markers and to explore the applicability of these markers for human studies.

show abstract

Section: Resultssupporting

confidence: 93%

“…37 and Molloy et al 42 have reported similar changes on tamoxifen treatment in the same mouse model for EGFR and the IRS-1 pathway, respectively (measured by immunoassay).…”

Section: Research Articlesmentioning

confidence: 72%

A Proteomic Analysis of the Plasma Glycoproteins of a MCF-7 Mouse Xenograft: A Model System for the Detection of Tumor Markers

et al. 2008

View full text Add to dashboard Cite

show abstract

“…In addition, further examination identified 229 differentially expressed genes that showed comparable changes in the EE and MIX groups but were not affected by TAM. Therefore, competition for ER binding (Robertson et al 1982, Mnif et al 2007) and downregulation of ER expression (Koibuchi et al 2000) do not sufficiently explain the gene expression effects resulting in the inhibition of ER-mediated, EE-induced UWW increases.…”

Section: Discussionmentioning

confidence: 99%

Effects of tamoxifen and ethynylestradiol cotreatment on uterine gene expression in immature, ovariectomized mice

Fong

Burgoon

Williams³

et al. 2010

Journal of Molecular Endocrinology

View full text Add to dashboard Cite

Tamoxifen (TAM), the primary treatment for estrogen receptor (ER)-positive breast cancer, has been associated with an increased incidence of endometrial cancer in postmenopausal, but not premenopausal women. TAM elicits a partial ER-mediated uterotrophic response in immature rodents when compared with ethynylestradiol (EE), a potent ER agonist. However, cotreatment with 1000 mg/kg TAM antagonizes the uterotrophic effect induced by 30 mg/kg EE. To further investigate the anti-uterotrophic activity of TAM, immature, ovariectomized C57BL/6 mice were treated with a single oral dose of EE, TAM, EECTAM, or vehicle, and harvested at 2, 4, 8, 12, 18, and 24 h or after three daily treatments at 72 h. Significant increases in uterine wet weight (UWW) were observed at 18 h for EE, TAM, and the mixture. However, mixture induction of UWW was significantly lower when compared with EE-induced uterotrophy at 72 h. This inhibitory effect is also reflected in decreases in luminal circumference, yet EE-induced luminal epithelial cell height was unaffected by cotreatment with TAM. Gene expression analysis using a 2!2 factorial cDNA microarray study design identified 2518 differentially expressed genes following EE treatment alone. However, only 290 EE-elicited gene expression changes were affected by TAM cotreatment, in a manner consistent with the anti-estrogenic response. These data suggest that TAM antagonism of EE-induced UWW increase involves the selective inhibition of EE-induced genes.

show abstract

“…The MCF-7 cell line was among the first ER-positive human breast cancer cell lines to be characterized as responsive to the mitogenic effects of estrogens in cell culture, as well as in athymic nude mice bearing MCF-7 cell xenografts [ 35 - 37 ]. Further, MCF-7 cells demonstrate estrogen-stimulated expression of a number of well-characterized estrogen-responsive genes, including Cathepsin D and pS2 [ 14 ].…”

Section: Discussionmentioning

confidence: 99%

High-throughput cell-based screening reveals a role for ZNF131 as a repressor of ERalpha signaling

et al. 2008

View full text Add to dashboard Cite

Background: Estrogen receptor α (ERα) is a transcription factor whose activity is affected by multiple regulatory cofactors. In an effort to identify the human genes involved in the regulation of ERα, we constructed a high-throughput, cell-based, functional screening platform by linking a response element (ERE) with a reporter gene. This allowed the cellular activity of ERα, in cells cotransfected with the candidate gene, to be quantified in the presence or absence of its cognate ligand E2.

show abstract

Regulation of estrogen receptor and epidermal growth factor receptor by tamoxifen under high and low estrogen environments in MCF-7 cells grown in athymic mice.

Cited by 8 publications

References 0 publications

A Proteomic Analysis of the Plasma Glycoproteins of a MCF-7 Mouse Xenograft: A Model System for the Detection of Tumor Markers

A Proteomic Analysis of the Plasma Glycoproteins of a MCF-7 Mouse Xenograft: A Model System for the Detection of Tumor Markers

Effects of tamoxifen and ethynylestradiol cotreatment on uterine gene expression in immature, ovariectomized mice

High-throughput cell-based screening reveals a role for ZNF131 as a repressor of ERalpha signaling

Contact Info

Product

Resources

About