Coalition of Nuclear Receptors in the Nervous System

Förthmann, Benjamin; Aletta, John M.; Lee, Yu Wei; Terranova, Christopher; Birkaya, Barbara; Stachowiak, Ewa K.; Stachowiak, Michal K.; Claus, Piet

doi:10.1002/jcp.25036

Cited by 11 publications

(10 citation statements)

References 51 publications

(95 reference statements)

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“…Fibroblast growth factor signaling is also engaged in neural stem cell regulation, neurogenesis, and cross talk with neurotrophic signaling. [211][212][213][214] Remarkably, FGF2 can transform embryonic stem cells to neural crest stem cells, further confirming the role of FGF signaling in neural crest development. 102 Among the four FGFR receptors, only FGFR1 and FGFR2 are expressed in the salivary glands, where they regulate salivary branching morphogenesis and cell survival.…”

Section: Receptor Tyrosine Kinases As Stemness Targets In Adenoid Cysmentioning

confidence: 66%

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Clinical and molecular insights into adenoid cystic carcinoma: Neural crest‐like stemness as a target

Yarbrough

Panaccione

Chang

et al. 2016

Laryngoscope Investig Oto

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ObjectivesThis review surveys trialed therapies and molecular defects in adenoid cystic carcinoma (ACC), with an emphasis on neural crest‐like stemness characteristics of newly discovered cancer stem cells (CSCs) and therapies that may target these CSCs.Data SourcesArticles available on Pubmed or OVID MEDLINE databases and unpublished data.Review MethodsSystematic review of articles pertaining to ACC and neural crest‐like stem cells.ResultsAdenoid cystic carcinoma of the salivary gland is a slowly growing but relentless cancer that is prone to nerve invasion and metastases. A lack of understanding of molecular etiology and absence of targetable drivers has limited therapy for patients with ACC to surgery and radiation. Currently, no curative treatments are available for patients with metastatic disease, which highlights the need for effective new therapies. Research in this area has been inhibited by the lack of validated cell lines and a paucity of clinically useful markers. The ACC research environment has recently improved, thanks to the introduction of novel tools, technologies, approaches, and models. Improved understanding of ACC suggests that neural crest‐like stemness is a major target in this rare tumor. New cell culture techniques and patient‐derived xenografts provide tools for preclinical testing.ConclusionPreclinical research has not identified effective targets in ACC, as confirmed by the large number of failed clinical trials. New molecular data suggest that drivers of neural crest‐like stemness may be required for maintenance of ACC; as such, CSCs are a target for therapy of ACC.

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Section: Receptor Tyrosine Kinases As Stemness Targets In Adenoid Cysmentioning

confidence: 66%

“…Fibroblast growth factor signaling is also engaged in neural stem cell regulation, neurogenesis, and cross talk with neurotrophic signaling . Remarkably, FGF2 can transform embryonic stem cells to neural crest stem cells, further confirming the role of FGF signaling in neural crest development .…”

Section: Resultsmentioning

confidence: 82%

Clinical and molecular insights into adenoid cystic carcinoma: Neural crest‐like stemness as a target

Yarbrough

Panaccione

Chang

et al. 2016

Laryngoscope Investig Oto

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“…Additionally, the high mRNA levels of the NHR coactivators NCOA1 and NCOA2 also correlated to a favorable NB disease ( Datasets S4 and S5 ) potentially by increasing the activity of NHRs, which may contribute to neural differentiation. Importantly, several human NHRs [e.g., NR1D1 ( 64 ), NR2E1 ( 65 ), NR5A1 ( 66 ), as well as RAR and RXR ( 67 )] are implicated in neurogenesis, maintenance, and a functional neuronal system. The significance of NHRs is further highlighted by the fact that 7 of 18 NHRs are linked to neuronal remodeling in Drosophila melanogaster ( 68 ).…”

Section: Discussionmentioning

confidence: 99%

MYCN -amplified neuroblastoma maintains an aggressive and undifferentiated phenotype by deregulation of estrogen and NGF signaling

Dzieran

Garcia

Westermark

et al. 2018

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

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SignificanceHigh-risk neuroblastoma (NB), a cancer of the sympathetic nervous system, is challenging to treat. MYCN is frequently amplified in high-risk NB and is linked to an undifferentiated phenotype and poor prognosis. Estrogen and nerve growth factor (NGF) are inducers of neural differentiation, a process associated with a favorable disease. We show that MYCN suppresses estrogen receptor alpha (ERα) and thereby NGF signaling and neural differentiation. ERα overexpression is sufficient to interfere with different tumorigenic processes and tumor growth. In patients with NB, ERα expression correlates with several clinical markers for good prognosis. Importantly, not only ERα but also the majority of other nuclear hormone receptors are linked to favorable NB, suggesting a potential prognostic and therapeutic value for these proteins.

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“…Given that CBP interacts with a large variety of TFs, nFGFR1 can potentially act as a global master regulator that delivers the RA signal to a large number of genes, including those that lack an RXR or Nur‐related site (Fig B, Box 3). Indeed nFGFR1‐xdCBP complexes form even larger complexes with RXR, RAR, and orphan Nur receptors, as well as with CREB and other TFs (Forthmann et al, ; Stachowiak et al, ). nFGFR1 synergistically regulates transcription by these TFs at their targeted sequences: RARE, NBRE, NurRE, CRE, etc.…”

Section: Nfgfr1 Programs Development Of Pluripotent Stem Cellsmentioning

confidence: 99%

Evidence‐Based Theory for Integrated Genome Regulation of Ontogeny—An Unprecedented Role of Nuclear FGFR1 Signaling

Stachowiak

2016

Journal Cellular Physiology

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Genetic experiments have positioned the fgfr1 gene at the top of the gene hierarchy that governs gastrulation, as well as the subsequent development of the major body axes, nervous system, muscles, and bones, by affecting downstream genes that control the cell cycle, pluripotency, and differentiation, as well as microRNAs. Studies show that this regulation is executed by a single protein, the nuclear isoform of FGFR1 (nFGFR1), which integrates signals from development‐initiating factors, such as retinoic acid (RA), and operates at the interface of genomic and epigenomic information. nFGFR1 cooperates with a multitude of transcriptional factors (TFs), and targets thousands of genes encoding for mRNAs, as well as miRNAs in top ontogenic networks. nFGFR1 binds to the promoters of ancient proto‐oncogenes and tumor suppressor genes, in addition to binding to metazoan morphogens that delineate body axes, and construct the nervous system, as well as mesodermal and endodermal tissues. The discovery of pan‐ontogenic gene programming by integrative nuclear FGFR1 signaling (INFS) impacts our understanding of ontogeny, as well as developmental pathologies, and holds new promise for reconstructive medicine, and cancer therapy. J. Cell. Physiol. 231: 1199–1218, 2016. © 2016 The Authors. Journal of Cellular Physiology published by Wiley Periodicals, Inc.

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Coalition of Nuclear Receptors in the Nervous System

Cited by 11 publications

References 51 publications

Clinical and molecular insights into adenoid cystic carcinoma: Neural crest‐like stemness as a target

Clinical and molecular insights into adenoid cystic carcinoma: Neural crest‐like stemness as a target

MYCN -amplified neuroblastoma maintains an aggressive and undifferentiated phenotype by deregulation of estrogen and NGF signaling

Evidence‐Based Theory for Integrated Genome Regulation of Ontogeny—An Unprecedented Role of Nuclear FGFR1 Signaling

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