Epigenetic activation of Sox2 gene in the developing vertebrate neural plate

Bouzas, Santiago O.; Marini, Melisa; Torres-Zelada, Eliana F.; Buzzi, Ailin Leticia; Morales-Vicente, David A.; Strobl-Mazzulla, Pablo H.

doi:10.1091/mbc.e16-01-0042

Cited by 4 publications

(3 citation statements)

References 43 publications

(64 reference statements)

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“…Our data also suggest a high co-localization of activated STAT3 with SOX2+ cells in BCa. Another possible mechanism of Sox2 activation is epigenetic regulation; SOX2 can be activated by JMJD2A ( Bouzas et al., 2016 ), which is the demethylase of H3K9me3 and is often highly expressed in BCa ( Kogure et al., 2013 ).…”

Section: Discussionmentioning

confidence: 99%

SOX2 Is a Marker for Stem-like Tumor Cells in Bladder Cancer

et al. 2017

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SummaryIt has been reported that functionally distinct cancer stem cells (CSCs) exist in human bladder cancer (BCa). Here, we found that Sox2, a transcription factor that is well characterized as a marker for stem cells, is upregulated in both mouse and human BCa. Sox2 expression is absent in normal urothelial cells, but it begins to be expressed in pre-neoplastic bladder tumors and continues to be expressed in invasive mouse BCa. Using s as a reporter of Sox2 transcriptional expression, we demonstrated that Sox2-expressing cells mark a subpopulation of tumor cells that fuel the growth of established BCa. SOX2-positive cells also expressed other previously reported BCa CSC markers, including Keratin14 (KRT14) and CD44v6. Ablation of Sox2-expressing cells within primary invasive BCa led to enhanced tumor regression, supporting the essential role of SOX2-positive cells in regulating BCa maintenance and progression. Our data show that Sox2 is a marker of bladder CSCs and indicate it as a potential clinical target for BCa therapy.

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Section: Discussionmentioning

confidence: 99%

SOX2 Is a Marker for Stem-like Tumor Cells in Bladder Cancer

et al. 2017

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“…The epigenetic and molecular specification of each of these tissues is followed by morphogenetic events such as neural tube closure (NTC) and the epithelial to mesenchymal transition (EMT) of NC cells. Recent studies in chick, amphibian and mouse embryos have identified transcription factors that regulate ectodermal derivative fate specification (Buitrago-Delgado et al, 2015, Bouzas et al, 2016, Mach et al, 2016, Riddiford and Schlosser, 2016, Acloque et al, 2017, Simoes-Costa et al, 2015), NTC (Ray and Niswander, 2016a, Ray and Niswander, 2016b) and NC EMT (Rogers et al, 2013, Schiffmacher et al, 2014, Strobl-Mazzulla and Bronner, 2012). Comparative analysis of early transcriptional regulators shows that many have overlapping expression and directly or indirectly regulate the expression of specific adhesion molecules to control these processes (Ray and Niswander, 2016a, Fairchild et al, 2014, Fairchild and Gammill, 2013, Strobl-Mazzulla and Bronner, 2012).…”

Section: Introductionmentioning

confidence: 99%

A catenin-dependent balance between N-cadherin and E-cadherin controls neuroectodermal cell fate choices

Rogers¹,

Sorrells²,

Bronner³

2018

Mechanisms of Development

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Characterizing endogenous protein expression, interaction and function, this study identifies in vivo interactions and competitive balance between N-cadherin and E-cadherin in developing avian (Gallus gallus) neural and neural crest cells. Numerous cadherin proteins, including neural cadherin (Ncad) and epithelial cadherin (Ecad), are expressed in the developing neural plate as well as in neural crest cells as they delaminate from the newly closed neural tube. To clarify independent or coordinate function during development, we examined their expression in the cranial region. The results revealed surprising overlap and distinct localization of Ecad and Ncad in the neural tube. Using a proximity ligation assay and co-immunoprecipitation, we found that Ncad and Ecad formed heterotypic complexes in the developing neural tube, and that modulation of Ncad levels led to reciprocal gain or reduction of Ecad protein, which then alters ectodermal cell fate. Here, we demonstrate that the balance of Ecad and Ncad is dependent upon the availability of β-catenin proteins, and that alteration of either classical cadherin modifies the proportions of the neural crest and neuroectodermal cells that are specified.

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“…KDM4A (also known as JMJD2A) is a demethylase that targets histone H3K9me2/3 and H3K36me2/3 leading to transcriptional activation. KDM4A has been shown to play an important role in gene expression [ 43 ], cellular differentiation [ 44 , 45 ] and cancer [ 46 ]. Tan et al .…”

Section: Introductionmentioning

confidence: 99%

F-box proteins in epigenetic regulation of cancer

Shen

Spruck

2017

Oncotarget

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Epigenetic abnormalities are now realized as important as genetic alterations in contributing to the initiation and progression of cancer. Recent advancements in the cancer epigenetics field have identified extensive alterations of the epigenetic network in human cancers, including histone modifications and DNA methylation. F-box proteins, the substrate receptors of SCF (SKP1-Cullin1-F-box protein) E3 ubiquitin ligases, can directly and indirectly affect the balance of epigenetic regulation. In this brief review, we discuss our current understanding of F-box proteins in cellular epigenetic regulation and how dysregulation of these processes contribute to cancer development.

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Epigenetic activation of Sox2 gene in the developing vertebrate neural plate

Abstract: The in vivo requirement of the histone demethylase JmjD2A, together with the kinase MSK1, results in a series of epigenetic events necessary for early activation of Sox2 and subsequent neural fate commitment in vertebrates.

Cited by 4 publications

References 43 publications

SOX2 Is a Marker for Stem-like Tumor Cells in Bladder Cancer

SOX2 Is a Marker for Stem-like Tumor Cells in Bladder Cancer

A catenin-dependent balance between N-cadherin and E-cadherin controls neuroectodermal cell fate choices

F-box proteins in epigenetic regulation of cancer

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