Nitric Oxide Inhibits Selectively the 17β-Estradiol-Induced Gene Expression without Affecting Nongenomic Events in HeLa Cells

Marino, Maria; Ficca, Ramona; Ascenzi, Paolo; Trentalance, A.

doi:10.1006/bbrc.2001.5433

Cited by 20 publications

(25 citation statements)

References 40 publications

(53 reference statements)

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“…The differential requirement of Src/ PI3K or intracellular calcium for MAPK activation is also observed in diverse cell types [15,109,129]. Different PKC isoforms are rapidly activated by E2 in HepG2 and MCF7 cells [102]. As a whole, these studies indicate that the rapid actions of E2 depend on a number of conditions such as the set of signal transduction molecules and downstream targets present in the target cell, thus the responses are likely to be diverse.…”

Section: Estrogen Receptor Non-genomic Activ-itymentioning

confidence: 79%

“…These rapid events may be classified into four main signaling cascade: phospholipase C (PLC)/protein kinase C (PKCs) [100][101][102][103][104][105][106], Ras/Raf/MAPK [72,[107][108][109][110][111][112][113], phosphatidyl inositol 3 kinase (PI3K)/AKT [15,16,80,81,97,[114][115][116][117][118], and cAMP/ protein kinase A (PKA) [104,[119][120][121][122][123].…”

Section: Estrogen Receptor Non-genomic Activ-itymentioning

confidence: 99%

“…The mechanism(s) by which E2 exerts proliferative effects is assumed to be exclusively mediated by rapid membrane-starting actions [72,80,101,102,114,115]. E2 treatment of mammary-derived MCF-7 cells triggers the association of ER with Src and p85 leading to DNA synthesis [115].…”

Section: Cell Functions Regulated By Non-genomic Signalsmentioning

confidence: 99%

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Estrogen Signaling Multiple Pathways to Impact Gene Transcription

Marino¹,

Galluzzo

Ascenzi

2006

Self Cite

529

382

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Steroid hormones exert profound effects on cell growth, development, differentiation, and homeostasis. Their effects are mediated through specific intracellular steroid receptors that act via multiple mechanisms. Among others, the action mechanism starting upon 17 -estradiol (E2) binds to its receptors (ER) is considered a paradigmatic example of how steroid hormones function. Ligand-activated ER dimerizes and translocates in the nucleus where it recognizes specific hormone response elements located in or near promoter DNA regions of target genes. Behind the classical genomic mechanism shared with other steroid hormones, E2 also modulates gene expression by a second indirect mechanism that involves the interaction of ER with other transcription factors which, in turn, bind their cognate DNA elements. In this case, ER modulates the activities of transcription factors such as the activator protein (AP)-1, nuclear factor-B (NF-B) and stimulating protein-1 (Sp-1), by stabilizing DNA-protein complexes and/or recruiting co-activators. In addition, E2 binding to ER may also exert rapid actions that start with the activation of a variety of signal transduction pathways (e.g. ERK/MAPK, p38/MAPK, PI3K/AKT, PLC/PKC). The debate about the contribution of different ER-mediated signaling pathways to coordinate the expression of specific sets of genes is still open. This review will focus on the recent knowledge about the mechanism by which ERs regulate the expression of target genes and the emerging field of integration of membrane and nuclear receptor signaling, giving examples of the ways by which the genomic and non-genomic actions of ERs on target genes converge.

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Section: Estrogen Receptor Non-genomic Activ-itymentioning

confidence: 79%

Section: Estrogen Receptor Non-genomic Activ-itymentioning

confidence: 99%

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Estrogen Signaling Multiple Pathways to Impact Gene Transcription

Marino¹,

Galluzzo

Ascenzi

2006

Self Cite

529

382

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“…Among proteins regulated by NO, modulation of the estrogen receptor (ER) a by S-nitrosylation (Marino et al 2001, Garban et al 2005 has important repercussions in cell homeostasis. 17b-Estradiol (E2) binding to the cytosolic ER population (both ERa and ERb) induces conformational changes that facilitate ER homo/heterodimerization, nuclear translocation, and binding to specific DNA recognition sequences (i.e.…”

Section: Introductionmentioning

confidence: 99%

“…The nature of these pathways as well as the role played in cell functions differs between ERa and ERb. In particular, rapid signals generated from the E2-ERa complex drive cells into the cell cycle and represent the main determinants for the E2 proliferative/survival effects (Marino et al 2001(Marino et al , 2002(Marino et al , 2003. By contrast, rapid effects generated by the E2-ERb complex drive cells out of the cell cycle (Acconcia et al 2005a), representing the key to understanding the E2-induced anti-proliferative effects working both during differentiative processes and in some forms of human cancer (e.g.…”

Section: Introductionmentioning

confidence: 99%

Nitric oxide impairs the 17β-estradiol-induced apoptosis in human colon adenocarcinoma cells

Marino

Galluzzo

Leone

et al. 2006

Endocr Relat Cancer

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Nitric oxide (NO) and 17b-estradiol (E2) are both important in gastrointestinal health and disease. NO contributes to gastrointestinal motility as well as to inflammation and carcinogenic processes. By contrast, E2 reduces the incidence of colon adenoma and carcinoma by about 30%. We report the genomic and non-genomic E2-estrogen receptor (ER) b-induced effects in human colon adenocarcinoma. The effect of NO on ERb activities was also assessed. The E2-ERbdependent gene transcription was inhibited by exogenous NO, whereas some non-genomic E2-dependent effects (e.g. p38/MAP kinase), important for the activation of the apoptotic cascade, were unaffected by NO. However, NO impaired the E2-induced pro-apoptotic cascade in human colon adenocarcinoma cells by inhibiting caspase-3. The effects of NO may reflect chemical modification(s) of Cys residues present in the DNA recognition domain of ERb as well as in the caspase-3 active site. On the whole, high NO concentrations suppressed the E2 protective effects in the gastrointestinal tract, suggesting that the caspase-dependent apoptotic cascade may become critical under conditions of high redox stress such as occur under specific activation of the immune system by chronic infections or pathogen challenge.

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