Determination of Protein Interactome of Transcription Factor Sox2 in Embryonic Stem Cells Engineered for Inducible Expression of Four Reprogramming Factors

Gao, Zhiguang; Cox, Jesse L.; Gilmore, Joshua M.; Ormsbee, Briana D.; Mallanna, Sunil K.; Washburn, Michael P.; Rizzino, Angie

doi:10.1074/jbc.m111.320143

Cited by 63 publications

(91 citation statements)

References 39 publications

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“…Through the coupling of affinity purification methods with mass spectrometry technology, numerous co-binding proteins of the core pluripotency transcription factors have been identified [33][34][35][36][37][38][39][40]. Taken together, these studies reveal an extensive protein-protein interaction network which includes other ESC transcription regulators, chromatin remodeling and modifying factors, DNA methyltransferases and Polycomb group proteins (PcG).…”

Section: The Expanded Esc Pluripotency Networkmentioning

confidence: 97%

The transcriptional regulation of pluripotency

Yeo

2012

Cell Res

117

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Abbreviations: 2C (2-cell); 2i (two inhibitor); BMP4 (bone morphogenic protein 4); ChIP (chromatin immunoprecipitation); ChIP-seq (chromatin immunoprecipitation and sequencing); ESCs (embryonic stem cells); EpiSCs (Epiblast-derived stem cells); Fgf4 (fibroblast growth factor 4); hESCs (human embryonic stem cells); ICM (inner cell mass); iPSCs (induced pluripotent stem cells); LIF (leukemia inhibitory factor); lincRNA (large intergenic non-coding RNA); mESCs (mouse embryonic stem cells); miRNA (micro RNA); ncRNA (non-coding RNA); PcG (Polycomb group proteins); PGCs (primodial germ cells); POU (Pit-Oct-Unc); RNAi (RNA interference); RNA-seq (RNA sequencing); SCF (stem cell factor); siRNA (short interfering RNA); XaXa (double X-chromosome active); XaXi (single X-chromosome inactivated)The defining features of embryonic stem cells (ESCs) are their self-renewing and pluripotent capacities. Indeed, the ability to give rise into all cell types within the organism not only allows ESCs to function as an ideal in vitro tool to study embryonic development, but also offers great therapeutic potential within the field of regenerative medicine. However, it is also this same remarkable developmental plasticity that makes the efficient control of ESC differentiation into the desired cell type very difficult. Therefore, in order to harness ESCs for clinical applications, a detailed understanding of the molecular and cellular mechanisms controlling ESC pluripotency and lineage commitment is necessary. In this respect, through a variety of transcriptomic approaches, ESC pluripotency has been found to be regulated by a system of ESC-associated transcription factors; and the external signalling environment also acts as a key factor in modulating the ESC transcriptome. Here in this review, we summarize our current understanding of the transcriptional regulatory network in ESCs, discuss how the control of various signalling pathways could influence pluripotency, and provide a future outlook of ESC research.

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Section: The Expanded Esc Pluripotency Networkmentioning

confidence: 97%

The transcriptional regulation of pluripotency

Yeo

2012

Cell Res

117

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“…Although its function in tumorigenesis remains unknown, other members of the muscarinic cholinergic receptor family have been reported to exert oncogenic or tumor-suppressing functions depending on biologic context (27,28). SMARCD1 (also known as BAF60a) has been shown to interact with a wide repertoire of transcription factors, including Oct3/4, Sox2, Sox10, c-Fos/c-Jun, peroxisome proliferatoractivated receptor a, vitamin D receptor, glucocorticoid receptor, retinoid-related orphan receptor a, and androgen receptor, to modulate gene expression (29)(30)(31)(32)(33)(34)(35)(36)(37). To this end, SMARCD1 is required for maintaining the pluripotency of embryonic stem cells and Tbx1-driven expression of Wnt5a, a noncanonical Wnt ligand that promotes cell migration and invasion in gastric cancer (38)(39)(40).…”

Section: Discussionmentioning

confidence: 99%

Epigenetic Silencing of miR-490-3p Reactivates the Chromatin Remodeler SMARCD1 to PromoteHelicobacter pylori–Induced Gastric Carcinogenesis

et al. 2015

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Chromatin remodeling has emerged as a hallmark of gastric cancer, but the regulation of chromatin regulators other than genetic change is unknown. Helicobacter pylori causes epigenetic dysregulation to promote gastric carcinogenesis, but the roles and functions of microRNAs (miRNA) in this multistage cascade are not fully explored. In this study, miRNA expression in preneoplastic and neoplastic lesions in murine stomachs induced by H. pylori and N-methyl-N-nitrosourea (MNU) was profiled by miRNA expression array. miR-490-3p exhibited progressive downregulation in gastritis, intestinal metaplasia, and adenocarcinoma during H. pylori and MNU-induced gastric carcinogenesis. Significant downregulation of miR-490-3p was confirmed in human gastric cancer tissues in which its regulatory region was found to be hypermethylated. miR-490-3p exerted growth-and metastasis-suppressive effects on gastric cancer cells through directly targeting SMARCD1, a SWItch/ Sucrose NonFermentable (SWI/SNF) chromatin remodeling complex subunit. Knockdown of SMARCD1 significantly attenuated the protumorigenic effects of miR-490-3p inhibitor, whereas enforced expression of SMARCD1 promoted in vitro and in vivo oncogenic phenotypes of gastric cancer cells. SMARCD1 was markedly upregulated in gastric cancer in which its high expression was associated with shortened patients' survival independent of TNM staging. In conclusion, hypermethylation-mediated silencing of miR-490-3p reactivates SMARCD1 to confer malignant phenotypes, mechanistically linking H. pylori, chromatin remodeling, and gastric carcinogenesis. Cancer Res; 75(4); 754-65. Ó2014 AACR.

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“…In addition, the transcription factor Sox-2 regulates the complex transcriptional network that maintains the unique characteristics of embryonic stem cells [30] and the anti-apoptosis property of human cancer stem cells [31]. Literature data show that expression of both these transcription factors is modified in an expanding list of cancers [32,33]. In humans, the normal ovarian and FT epithelia are characterized by negative or weak Oct4 and Sox-2 expression, that are conversely greatly enhanced during malignant transformation [18,19].…”

Section: Discussionmentioning

confidence: 99%

Repeated ovarian stimulation does not affect the expression level of proteins involved in cell cycle control in mouse ovaries and fallopian tubes

Luigi

Rossi

Castellucci

et al. 2014

J Assist Reprod Genet

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Purpose To understand if repeated cycles (2-4 rounds) of gonadotropin stimulation could affect intracellular localization/ content of proteins controlling cell cycle progression in mouse fallopian tubes (FT) and ovaries. Methods FT and ovaries of estrous mice (control) and of stimulated mice were analyzed to detect Oct-3/4, Sox-2, p53, β-catenin, pAKT and cyclin D1 localization/content. Spindles and chromosome alignment were analyzed in ovulated oocytes. Results After round 4, FT and ovaries of control and stimulated groups showed no differences in Oct-3/4, Sox-2 and β-catenin localization nor in Oct-3/4, Sox-2, p53, β-catenin and pAKT contents. Cyclin D1 level increased significantly in FT of treated mice. Oocytes number decreased meanwhile frequency of abnormal meiotic spindles increased with treatments. Conclusions Repetitive stimulations affected oocyte spindle morphology but did not induce changes in a set of proteins involved in cell cycle progression, usually altered in ovarian cancer. The significant increase of cyclin D1 in the FT requires further investigation.

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Determination of Protein Interactome of Transcription Factor Sox2 in Embryonic Stem Cells Engineered for Inducible Expression of Four Reprogramming Factors

Cited by 63 publications

References 39 publications

The transcriptional regulation of pluripotency

The transcriptional regulation of pluripotency

Epigenetic Silencing of miR-490-3p Reactivates the Chromatin Remodeler SMARCD1 to PromoteHelicobacter pylori–Induced Gastric Carcinogenesis

Repeated ovarian stimulation does not affect the expression level of proteins involved in cell cycle control in mouse ovaries and fallopian tubes

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