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• W2122907454 abstract "This study examines the cooperative effects of a human estrogen receptor-α (ERα) isoform on estrogen (E2)-mediated gene activation in U2-OS osteosarcoma cells. Δ5ERα, an alternatively spliced ERα variant lacking exon 5, is coexpressed with normal ERα in several E2-responsive neoplastic tissues. However, the potential interactions of Δ5ERα with normal ERα have not been functionally characterized. Δ5ERα encodes the hormone-independent trans-activating function (AF-1), as well as the constitutive receptor dimerization and DNA-binding domains. It is generated by an alternate splice event that omits exon 5 and alters the reading frame of the resulting mRNA. The Δ5ERα protein is prematurely truncated and lacks the majority of the hormone-binding and activating function-2 (AF-2) domains. When Δ5ERα mammalian expression vector was transfected alone in human ERα/ERβ-negative osteosarcoma U2-OS cells, it had no effect on either basal or E2-mediated EREtk81Luc reporter transcriptional activity, while transfected cells expressing control normal ERα increased EREtk81Luc activity up to 20-fold in response to 10 nm E2. However, whenΔ 5ERα was cotransfected with normal ERα, both basal and E2-stimulated EREtk81Luc reporter activation were increased approximately 500% over levels observed when cells were transfected with ERα alone. Similar effects of Δ5ERα and normal ERα coexpression were observed using an E2-responsive human C3 promoter/luciferase reporter construct. The effects of Δ5ERα on normal ERα were further assessed in U2-OS cells stably transfected with normal ERα. Transfection of increasing amounts of Δ5ERα expression vector into[ ERα+]OS cells resulted in potentiation of E2-stimulated ERELuc activity in a synergistic, dose-dependent manner. Moreover, coexpression of Δ5ERα in[ ERα+]OS cells improved E2 sensitivity 100-fold over cells expressing ERα alone. Proliferation rates of stable U2-OS cell lines expressing Δ5ERα were significantly increased (P < 0.05), with cell doubling times reduced from 35 h in control parental U2-OS cells to 28 h in[Δ 5ERα]OS cells. However, growth rates were not affected by either E2 or tamoxifen treatment. Electromobility shift/supershift assays using nuclear extracts of U2-OS cells stably transfected with ERα and Δ5ERα confirmed the constitutive binding of Δ5ERα and ERα protein to estrogen-response element (ERE) sequence independent of E2 and also showed an increase inΔ 5ERα/ERα-ERE complexes with E2 treatment. These data are consistent with interactive effects of normal ERα and Δ5ERα on transcription from classic ERE gene promoters.Δ 5ERα appears to therefore act as a dominant positive receptor that increases both basal and E2-stimulated gene transactivation of normal ERα." @default.
• W2122907454 created "2016-06-24" @default.
• W2122907454 creator A5039338616 @default.
• W2122907454 creator A5043000133 @default.
• W2122907454 date "1998-09-01" @default.
• W2122907454 modified "2023-10-03" @default.
• W2122907454 title "A Tumor-Specific Truncated Estrogen Receptor Splice Variant Enhances Estrogen-Stimulated Gene Expression" @default.
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• W2122907454 doi "https://doi.org/10.1210/mend.12.9.0170" @default.
• W2122907454 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9731704" @default.
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