An estrogen-responsive element from the 5'-flanking region of the rat prolactin gene functions in MCF-7 but not in HeLa cells

Somasekhar, Madhu B.; Gorski, Jack

doi:10.1016/0378-1119(88)90374-5

Cited by 10 publications

(3 citation statements)

References 15 publications

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“…Further, we (51) and others (8,40,46,80,81) (4,22). MCF-7 cells were chosen for study since the cells permit a direct analysis of the action of mRXRI with respect to function of the endogenous ER (13,15,38,68,72 [34]). The preparation of mRXRI is described elsewhere (52).…”

mentioning

confidence: 99%

Inhibition of estrogen-responsive gene activation by the retinoid X receptor beta: evidence for multiple inhibitory pathways.

Segars¹,

Marks²,

Hirschfeld³

et al. 1993

Mol. Cell. Biol.

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The retinoid X receptor 13 (RXRI; H-2RIIBP) forms heterodimers with various nuclear hormone receptors and binds multiple hormone response elements, including the estrogen response element (ERE). In this report, we show that endogenous RXR3 contributes to ERE binding activity in nuclear extracts of the human breast cancer cell line MCF-7. To define a possible regulatory role of RXRf3 regarding estrogen-responsive transcription in breast cancer cells, RXRI3 and a reporter gene driven by the vitellogenin A2 ERE were transfected into estrogen-treated MCF-7 cells. RXR13 inhibited ERE-driven reporter activity in a dosedependent and element-specific fashion. This inhibition occurred in the absence of the RXR ligand 9-cis retinoic acid. The RXRB-induced inhibition was specific for estrogen receptor (ER)-mediated ERE activation because inhibition was observed in ER-negative MDA-MB-231 cells only following transfection of the estrogen-activated ER. No inhibition of the basal reporter activity was observed. The inhibition was not caused by simple competition of RXRI3 with the ER for ERE binding, since deletion mutants retaining DNA binding activity but lacking the N-terminal or C-terminal domain failed to inhibit reporter activity. In addition, cross-linking studies indicated the presence of an auxiliary nuclear factor present in MCF-7 cells that contributed to RXRI3 binding of the ERE. Studies using known heterodimerization partners of RXR13 confirmed that RXRP/ triiodothyronine receptor ai heterodimers avidly bind the ERE but revealed the existence of another triiodothyronine-independent pathway of ERE inhibition. These results indicate that estrogen-responsive genes may be negatively regulated by RXRI3 through two distinct pathways.

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mentioning

confidence: 99%

Inhibition of estrogen-responsive gene activation by the retinoid X receptor beta: evidence for multiple inhibitory pathways.

Segars¹,

Marks²,

Hirschfeld³

et al. 1993

Mol. Cell. Biol.

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“…In addition, mERR␣ can bind to the palindromic ERE as well as complex response elements containing multiple half-sites lacking the consensus 5Ј-flanking sequence (16). In some promoters, such as those regulating expression of the oxytocin (25), prolactin (30), and lactoferrin (39) genes, a putative ERRE overlaps a known ERE: a potential physiologic role of ERR␣ may be to modulate the hormone responsiveness of a subset of estrogen receptor target genes (16,39).…”

Section: Discussionmentioning

confidence: 99%

The Orphan Nuclear Receptor Estrogen-Related Receptor α Is a Transcriptional Regulator of the Human Medium-Chain Acyl Coenzyme A Dehydrogenase Gene

Sladek

Bader

Giguère

1997

Molecular and Cellular Biology

343

330

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Estrogen-related receptor ␣ (ERR␣) is an orphan member of the superfamily of nuclear hormone receptors. ERR␣ was initially isolated based on its sequence homology to the estrogen receptor but is not activated by classic estrogens. To identify possible physiologic functions for this orphan receptor, we cloned the mouse ERR␣ cDNA and used it to characterize the expression of ERR␣ transcripts and to identify potential ERR␣ target genes. RNA in situ hybridization studies detect ERR␣ transcripts in an organ-specific manner through mid-to late embryonic development, with persistent high-level expression in brown adipose tissue and intestinal mucosa. In the adult mouse, ERR␣ is most highly expressed in kidney, heart, and brown adipocytes, tissues which preferentially metabolize fatty acids. Binding site selection experiments show that ERR␣ preferentially binds to an ERR␣ response element ( The orphan nuclear receptor estrogen-related receptor ␣ (ERR␣) was initially cloned by low-stringency screening of a human kidney library with an estrogen receptor DNA binding domain probe (12). Subsequently, protein micropurification and microsequencing techniques identified ERR␣ as a repressor of the simian virus 40 major late promoter and implicated the receptor as a key regulator of the early-to-late switch of simian virus 40 gene expression (35). ERR␣ has also been shown to accentuate estrogen-dependent induction of the complex lactoferrin estrogen response element (ERE), possibly by forming heterodimers with the estrogen receptor (39). While ERR␣ displays significant homology to the estrogen receptor, it does not bind estrogens in vitro, nor is its transcriptional activity modulated by estrogens (12, 39). Like many other members of the nuclear receptor superfamily, ERR␣ has no known ligand and is therefore considered an orphan receptor. In the absence of an associated ligand, one approach to uncovering potential physiologic roles for ERR␣ is to identify possible target genes.

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“…(melanoma murino), MCF--7 (câncer de mama) e uma linhagem normal NIH/3T3 (fibroblasto murino) obtidas do banco de células ATCC. Essas linhagens são muito utilizadas como modelos experimentais em diversos estudos em todo o mundo e possuem algumas características marcantes como a capacidade de crescer aderidas ao substrato, não apresentarem caspase--3 (Janicke 1998) e responderem diferentemente à presença de estrógeno ( Somasekhar & Gorski, 1988;Levenson & Jordan, 1997).…”

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Caracterização da atividade citotóxica da peçonha de Bothrops marmoratus e efeitos de uma PLA2-Lys49 isolada sobre células de adenocarcinoma cervical (Hela) : do transcriptoma ao proteoma

Macêdo¹

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AGRADECIMENTOS "Quem caminha sozinho pode até chegar mais rápido, mas aquele que vai acompanhado, com certeza vai mais longe." Clarice Lispector Agradeço em primeiro lugar а Deus que iluminou о meu caminho durante todo esse tempo e me deu saúde, força е coragem. À Profa. Dra. Mariana de Souza Castro pelos ensinamentos e confiança mais uma vez. E por ter me incentivado a literalmente ir mais longe. Ao Dr. Jay W. Fox da Universidade da Virgínia pelos ensinamentos, pelas inúmeras oportunidades, confiança, cuidado e carinho inesquecíveis. Agradeço também aos outros colaboradores de seu laboratório, Julie Burns, Drs. John Shannon, Erin Jeffery e Nicholas Sherman. Ao Prof. Dr. Osmindo Rodrigues Pires Jr. pelos ensinamentos e por estar sempre, sempre presente quando precisei. À prof. Msc. Marta Regina Magalhães do CEPB-PUC Goiás por novamente fornecer a peçonha, sem a qual esse trabalho seria impossível.

show abstract

An estrogen-responsive element from the 5'-flanking region of the rat prolactin gene functions in MCF-7 but not in HeLa cells

Cited by 10 publications

References 15 publications

Inhibition of estrogen-responsive gene activation by the retinoid X receptor beta: evidence for multiple inhibitory pathways.

Inhibition of estrogen-responsive gene activation by the retinoid X receptor beta: evidence for multiple inhibitory pathways.

The Orphan Nuclear Receptor Estrogen-Related Receptor α Is a Transcriptional Regulator of the Human Medium-Chain Acyl Coenzyme A Dehydrogenase Gene

Caracterização da atividade citotóxica da peçonha de Bothrops marmoratus e efeitos de uma PLA2-Lys49 isolada sobre células de adenocarcinoma cervical (Hela) : do transcriptoma ao proteoma

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