Estrogen upregulation of BRCA1 expression with no effect on localization

Romagnolo, Donato F.; Annab, Lois A.; Thompson, Tracy E.; Risinger, John I.; Terry, Lori; Barrett, J. Carl; Afshari, Cynthia A.

doi:10.1002/(sici)1098-2744(199806)22:2<102::aid-mc5>3.0.co;2-o

Cited by 58 publications

(53 citation statements)

References 35 publications

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“…Elsewhere, the expression of BRCA1 mRNA was induced from 2.5-to 5.0-fold by oestrogen in human breast cancer cell lines MCF7, and the BRCA1 protein was about three-fold (Romagnolo et al, 1998). In our work, we found a comparable increase, of two-to four-fold for BRCA1 and BRCA2 mRNA, by resveratrol in human breast cell lines MCF7, MDA-MB 231 and HBL 100.…”

Section: Discussionsupporting

confidence: 69%

Resveratrol increases BRCA1 and BRCA2 mRNA expression in breast tumour cell lines

et al. 2003

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The phytochemical resveratrol, found in grapes, berries and peanuts, has been found to possess cancer chemopreventive effects by inhibiting diverse cellular events associated with tumour initiation, promotion and progression. Resveratrol is also a phyto-oestrogen, binds to and activates oestrogen receptors that regulate the transcription of oestrogen-responsive target genes such as the breast cancer susceptibility genes BRCA1 and BRCA2. We investigated the effects of resveratrol on BRCA1 and BRCA2 expression in human breast cancer cell lines (MCF7, HBL 100 and MDA-MB 231) using quantitative real-time RT -PCR, and by perfusion chromatography of the proteins. All cell lines were treated with 30 mM resveratrol. The expressions of BRCA1 and BRCA2 mRNAs were increased although no change in the expression of the proteins were found. These data indicate that resveratrol at 30 mM can increase expression of genes involved in the aggressiveness of human breast tumour cell lines.

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Section: Discussionsupporting

confidence: 69%

Resveratrol increases BRCA1 and BRCA2 mRNA expression in breast tumour cell lines

et al. 2003

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“…Conversely, expression of BRCA-1 in breast ER-negative (HBL-100 and MDA-MD-231) cancer cells was not influenced by estrogen, suggesting that ER status may be important for regulation of BRCA-1. The antiestrogen ICI-182780 inhibited estrogen-induced cell proliferation and BRCA-1 expression in ER-positive cells, thus confirming the participation of the ER pathway [Romagnolo et al, 1998]. …”

Section: Disruption Of Brca-1 Expression By Ahr-ligandsmentioning

confidence: 78%

Epigenetics of breast cancer: Polycyclic aromatic hydrocarbons as risk factors

Jeffy

Chirnomas

Romagnolo

2002

Environ and Mol Mutagen

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In the absence of a causal relationship between the incidence of sporadic breast cancer and occurrence of mutations in breast cancer susceptibility genes, efforts directed to investigating the contribution of environmental xenobiotics in the etiology of sporadic mammary neoplasia are warranted. Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous pollutants, which have been shown to induce DNA damage and disrupt cell cycle progression. In this report we discuss published data pointing to PAHs as a risk factor in carcinogenesis, and present findings generated in our laboratory suggesting that the mammary tumorigenicity of PAHs may be attributable, at least in part, to disruption of BRCA-1 expression by reactive PAHmetabolites. We report that benzo[a]pyrene (B[a]P), selected as a prototype PAH, disrupts BRCA-1 transcription in estrogen receptor (ER)-positive but not ER-negative breast cancer cells. The reduced potential for BRCA-1 expression in B[a]Ptreated cells coincides with disruption of cell cycle kinetics and accumulation of p53. These effects are counteracted by the AhR-antagonist ␣-naphthoflavone (ANF), and in breast cancer cells expressing mutant p53 or the E6 human papilloma virus protein. We suggest that exposure to PAHs may be a predisposing factor in the etiology of sporadic breast cancer by disrupting the expression of BRCA-1. Environ. Mol. Mutagen. 39:235-244, 2002.

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“…To investigate whether induction of BRCA1 expression was associated with changes in the 3C profile, we examined the effect of stimulating MCF7 cells with estrogen (␤-estradiol; E2). This treatment induces BRCA1 mRNA levels (21,22), indirectly through associated changes in cell proliferation (23). We therefore analyzed BRCA1 transcription levels in MCF7 cells either without E2 (defined media as above) or after 5 and 24 h of E2 stimulation.…”

Section: The Association Between 5 and 3 Ends Of Brca1 Is Lost Upon Ementioning

confidence: 99%

Dynamic interactions between the promoter and terminator regions of the mammalian BRCA1 gene

Tan-Wong

French

Proudfoot

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

134

121

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The 85-kb breast cancer-associated gene BRCA1 is an established tumor suppressor gene, but its regulation is poorly understood. We demonstrate by gene conformation analysis in both human cell lines and mouse mammary tissue that gene loops are imposed on BRCA1 between the promoter, introns, and terminator region. Significantly, association between the BRCA1 promoter and terminator regions change upon estrogen stimulation and during lactational development. Loop formation is transcription-dependent, suggesting that transcriptional elongation plays an active role in BRCA1 loop formation. We show that the BRCA1 terminator region can suppress estrogen-induced transcription and so may regulate BRCA1 expression. Significantly, BRCA1 promoter and terminator interactions vary in different breast cancer cell lines, indicating that defects in BRCA1 chromatin structure may contribute to dysregulated expression of BRCA1 seen in breast tumors.transcriptional regulation ͉ chromatin conformation ͉ gene repression ͉ mammary gland ͉ breast cancer E xpression of the tumor suppressor gene BRCA1 is reduced in a significant proportion of human breast tumors (1-3). Although up to one-third of these cases can be explained by promoter hypermethylation (4, 5) for most cases the cause is unknown. Understanding the underlying mechanisms of BRCA1 gene repression is critical for generating effective strategies for re-establishing BRCA1 expression and thus restoring its tumor suppressor function.Transcriptional initiation of protein-coding genes depends on a coordinated interplay of protein-DNA and protein-protein interactions (6). In addition to the assembly of RNA polymerase II (Pol II) with basal transcription machinery on the gene promoter, numerous transcription factors are recruited to either activate or repress transcription. As many of these factors associate with DNA sequences distant to the promoter, transcriptional regulation often involves long-range DNA associations, possibly mediated by the formation of chromatin loops (7). Chromatin loops can be detected by the chromosome conformation capture (3C) technique (8), which involves formaldehyde cross-linking of chromatin in live cells, digesting DNA with restriction enzymes, and then religating DNA in dilute solution to favor intramolecular ligation. PCR is then used to detect the presence of such ligation products. 3C has been used to study the normal regulation of genes in multiple eukaryotic species and supports a looping model for gene activation and repression. For example, transcriptional activation of the ␤-globin gene in mouse is associated with interactions between multiple hypersensitive sites spanning Ͼ50 kb of DNA (9), whereas repression of the maternal IGF2 gene is linked to a long-range association between IGF2 and H19 loci, restricting access to an IGF2 enhancer (10).Several human diseases are associated with mutations in long-range control elements (11). Examples include Campomelic dysplasia, which can be caused by deletion of critical regulatory elements Ϸ50 kb upst...

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Estrogen upregulation of BRCA1 expression with no effect on localization

Cited by 58 publications

References 35 publications

Resveratrol increases BRCA1 and BRCA2 mRNA expression in breast tumour cell lines

Resveratrol increases BRCA1 and BRCA2 mRNA expression in breast tumour cell lines

Epigenetics of breast cancer: Polycyclic aromatic hydrocarbons as risk factors

Dynamic interactions between the promoter and terminator regions of the mammalian BRCA1 gene

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