Insulin-like growth factors activate estrogen receptor to control the growth and differentiation of the human neuroblastoma cell line SK-ER3.

Q, Z; Santagati, Sabrina; Patrone, Cesare; Pollio, Giuseppe; Vegeto, Elisabetta; Maggi, Adriana

doi:10.1210/mend.8.7.7984152

Cited by 68 publications

(43 citation statements)

References 16 publications

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“…Previous work from our laboratory demonstrated the existence of a crosscoupling between ER␣ and insulin growth factor in neural cells (7,8) subsequently confirmed by several other groups (9 -11). In addition, ERs co-localize with receptor tyrosine kinases (RTKs), such as insulin growth factor receptor or EGFR, in several areas of the developing and adult nervous system (5,12,13), and functional interactions between ERs and RTKs have been documented (7)(8)(9)(10)14).…”

supporting

confidence: 64%

Estrogen Receptor α, a Molecular Switch Converting Transforming Growth Factor-α-mediated Proliferation into Differentiation in Neuroblastoma Cells

Ciana¹,

Ghisletti²,

Mussi³

et al. 2003

Journal of Biological Chemistry

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Transforming growth factor-␣ (TGF-␣) is known to promote both proliferation and differentiation of neural cell progenitors. Using the human neuroblastoma cell line SK-N-BE that is induced to proliferate by TGF-␣, we demonstrated that the expression of a single transcription factor, the estrogen receptor-␣ (ER␣), can reroute the TGF-␣ mitogenic signaling toward a path leading to differentiation. With selected mutations in ER␣ and signal transducer and activator of transcription 3 (Stat3), we demonstrated that the blockade of TGF-␣ mitotic potential was not dependent on ER␣ DNA binding activity but required a transcriptionally active Stat3. In neuroblastoma cells, 17␤-estradiol treatment induced a transient increase in the transcription of estrogen-responsive element-containing promoters including those regulating TGF-␣ and prothymosin ␣ synthesis. Based on the data presented, we hypothesized that in the presence of prothymosin ␣, ER␣ activates its direct target genes and increases cell proliferation, whereas in the presence of high levels of TGF-␣, ER␣ preferentially interacts with Stat3 and causes cell differentiation. Our results reveal a novel form of "end-product" regulation of an intracellular receptor that occurs through recruitment of membrane receptors and their signaling effector system. Cross-coupling between membrane and intracellular receptors has been described by several laboratories. This study proves the relevance of these interactions in cellular responses to growth factors.

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supporting

confidence: 64%

Estrogen Receptor α, a Molecular Switch Converting Transforming Growth Factor-α-mediated Proliferation into Differentiation in Neuroblastoma Cells

Ciana¹,

Ghisletti²,

Mussi³

et al. 2003

Journal of Biological Chemistry

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“…In different cell lines, including neuroblastoma cells (Ma et al 1994), IGF-I may activate oestrogen receptors in the absence of oestradiol. Whether or not this is also valid for the brain in vivo is unknown.…”

Section: Mechanisms Of Crosstalk Between Oestradiol and Igf-i In The mentioning

confidence: 99%

Interdependence of oestrogen and insulin-like growth factor-I in the brain: potential for analysing neuroprotective mechanisms

Méndez

Azcoitia²,

Garcia-Segura

2005

Journal of Endocrinology

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The actions of oestradiol in the brain involve interaction with growth factors, such as insulin-like growth factor-I (IGF-I). Many cells in the brain co-express receptors for oestradiol and IGF-I and both factors interact to regulate neural function. The relationship of oestrogen receptor with IGF-I receptor through the mitogen-activated protein kinase and the phosphoinositide 3-kinase signalling pathways may represent the point of convergence used by these two factors to cooperatively modulate neuritic growth, synaptic plasticity, neuroendocrine events, reproductive behaviour and neuronal survival. In addition, Akt and glycogen synthase kinase 3 are key molecular targets to explain the interaction of oestrogen and IGF-I receptor signalling in the promotion of neuroprotection.

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“…In addition to the traditional mode of nuclear receptor transactivation, there is accumulating evidence that receptors on the cell surface initiate signals that alter nuclear receptor activity. For example, epidermal growth factor (Kato et al 1995, Bunone 1996, transforming growth factor a (Ignar- Trowbridge et al 1993), and insulin-like growth factor-I (Ma et al 1994) are able to alter the capacity of nuclear receptors to activate gene expression. This nonclassical mode of nuclear receptor regulation can be hormone independent or hormone dependent and provides a link between various cues received by receptors on the cell surface and the activity of receptors in the nucleus.…”

Section: Introductionmentioning

confidence: 99%

Rho GDP dissociation inhibitor α interacts with estrogen receptor α and influences estrogen responsiveness

Marzouk

Schultz-Norton

Likhite

et al. 2007

Journal of Molecular Endocrinology

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Estrogen receptor a (ERa) is a ligand-activated transcription factor that regulates expression of estrogen-responsive genes. Upon binding of the ligand-occupied ERa to estrogen response elements (EREs) in DNA, the receptor interacts with a variety of coregulatory proteins to modulate transcription of target genes. We have isolated and identified a number of proteins associated with the DNA-bound ERa. One of these proteins, Rho guanosine diphosphate (GDP) dissociation inhibitor a (RhoGDIa), is a negative regulator of the Rho family of GTP-binding proteins. In this study, we demonstrate that endogenously expressed RhoGDIa is present in the nucleus as well as the cytoplasm of MCF-7 breast cancer cells, and that RhoGDIa binds directly to ERa, alters the ERa-ERE interaction, and influences the ability of ERa to regulate transcription of a heterologous estrogen-responsive reporter plasmid in transient transfection assays as well as endogenous, estrogen-responsive genes in MCF-7 cells. Our studies suggest that, in addition to the activity of RhoGDIa in the cytoplasm, it also influences ERa signaling in the nucleus.

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Insulin-like growth factors activate estrogen receptor to control the growth and differentiation of the human neuroblastoma cell line SK-ER3.

Cited by 68 publications

References 16 publications

Estrogen Receptor α, a Molecular Switch Converting Transforming Growth Factor-α-mediated Proliferation into Differentiation in Neuroblastoma Cells

Estrogen Receptor α, a Molecular Switch Converting Transforming Growth Factor-α-mediated Proliferation into Differentiation in Neuroblastoma Cells

Interdependence of oestrogen and insulin-like growth factor-I in the brain: potential for analysing neuroprotective mechanisms

Rho GDP dissociation inhibitor α interacts with estrogen receptor α and influences estrogen responsiveness

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