Nanog transforms NIH3T3 cells and targets cell-type restricted genes

Piestun, Dan; Kochupurakkal, Bose; Jacob‐Hirsch, Jasmine; Zeligson, Sharon; Koudritsky, Mark; Domany, Eytan; Amariglio, Ninette; Rechavi, Gideon; Givol, David

doi:10.1016/j.bbrc.2006.02.152

Cited by 71 publications

(70 citation statements)

References 21 publications

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“…One possibility is that Nanog shares different targets between porcine embryos and fibroblasts. Microarray analysis confirms that there is very little overlap of Nanog's target genes in cell lines derived from different tissues, suggesting that Nanog's target genes are variable in a tissue specific manner (Piestun et al, 2006). The genome is demethylated in ESCs and embryos, so Nanog is prone to occupy its target sites in many promoters (Boyer et al, 2005).…”

Section: Discussion Transient Elevation Of Nanog Expression Can Activmentioning

confidence: 88%

Overexpression Nanog Activates Pluripotent Genes in Porcine Fetal Fibroblasts and Nuclear Transfer Embryos

Zhang

Luo

Bou

et al. 2011

The Anatomical Record

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Nanog as an important transcription factor plays a pivotal role in maintaining pluripotency and in reprogramming the epigenome of somatic cells. Its ability to function on committed somatic cells and embryos has been well defined in mouse and human, but rarely in pig. To better understand Nanog's function on reprogramming in porcine fetal fibroblast (PFF) and nuclear transfer (NT) embryo, we cloned porcine Nanog CDS and constructed pcDNA3.1 (þ)/Nanog and pEGFP-C1/Nanog overexpression vectors and transfected them into PFFs. We studied the cell biological changes and the expression of Nanog, Oct4, Sox2, Klf4, C-myc, and Sall4 in transfected PFFs. We also detected the development potential of the cloned embryos harboring Nanog stably overexpressed fibroblasts and the expression of Oct4, Sox2, and both endogenous and exogenous Nanog in these embryos. The results showed that transient overexpression Nanog in PFF could activate the expression of Oct4 (5-fold), C-myc (2-fold), and Sall4 (5-fold) in somatic cells, but they could not be maintained during G418 selection. In NT embryos, although Nanog overexpression did not have a significant effect on blastocyst development rate and blastocyst cell number, it could significantly activate the expression of endogenous Nanog, Oct4, Sox2 to 160-fold, 93-fold, and 182-fold, respectively (P < 0.05). Our results demonstrate that Nanog could interact with and activate other pluripotent genes both in PFFs and embryos. Anat Rec, 294:1809Rec, 294: -1817Rec, 294: , 2011. V V C 2011 Wiley-Liss, Inc.

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Section: Discussion Transient Elevation Of Nanog Expression Can Activmentioning

confidence: 88%

Overexpression Nanog Activates Pluripotent Genes in Porcine Fetal Fibroblasts and Nuclear Transfer Embryos

Zhang

Luo

Bou

et al. 2011

The Anatomical Record

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“…These results and ours suggest that Nanog expression can be augmented in early-stage differentiation of both ES cells and EC cells such as F9 cells. The physiological implication of the increased Nanog expression at the early stage of differentiation is not clear, but we speculate that it might be related to proliferation and survival of the early differentiating cells; NIH3T3 fibroblast cells overexpressing Nanog occur in a greater number in S phase than naïve NIH3T3 cells (Zhang et al, 2005;Piestun et al, 2006). Ectopic expression of Nanog in both human and mouse ES cells facilitates the transition from inner cell mass to primitive ectoderm by promoting cell survival (Darr et al, 2006).…”

Section: Discussionmentioning

confidence: 96%

The phosphoinositide-3-kinase/Akt pathway mediates the transient increase in Nanog expression during differentiation of F9 cells

Kim

et al. 2010

Arch. Pharm. Res.

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Nanog is a key determinant that maintains self-renewal and pluripotency of embryonic stem cells and represses their differentiation to endoderm. In this study, we examined the regulation of Nanog expression by phosphoinositide-3-kinase (PI3K)/Akt pathway during retinoic acid (RA)-induced differentiation of F9 embryonic carcinoma cells. Nanog protein expression was transiently upregulated up to 6 h after RA treatment and then declined. In agreement, a murine Nanog promoter reporter assay revealed that promoter activity increased during early stage of differentiation, but decreased when F9 cells became fully differentiated. RA treatment of F9 cells also led to a transient and parallel increase in both Akt and glycogen synthase kinase 3β phosphorylations. Nanog expression was diminished in the early stage by LY294002, a PI3K inhibitor, but was not affected in the late stage despite considerable inhibition of Akt phosphorylation and endoderm marker expression by the inhibitor. These data suggest that RA-induced PI3K/Akt activation in the early stage of differentiation is required for Nanog expression, which becomes independent of PI3K/Akt signaling once the differentiation is established. Thus, Nanog expression appears to be differently regulated by the PI3K/ Akt pathway depending on differentiation stage.

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“…The overexpression of Nanog promotes recurrence in cisplatin -treated oral squamous cell carcinoma patients and was found to induce the transformation of NIH3T3 cells [22,23].…”

Section: Introductionmentioning

confidence: 99%

Association of differential β‐catenin expression with Oct‐4 and Nanog in oral squamous cell carcinoma and their correlation with clinicopathological factors and prognosis

et al. 2014

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Nanog transforms NIH3T3 cells and targets cell-type restricted genes

Cited by 71 publications

References 21 publications

Overexpression Nanog Activates Pluripotent Genes in Porcine Fetal Fibroblasts and Nuclear Transfer Embryos

Overexpression Nanog Activates Pluripotent Genes in Porcine Fetal Fibroblasts and Nuclear Transfer Embryos

The phosphoinositide-3-kinase/Akt pathway mediates the transient increase in Nanog expression during differentiation of F9 cells

Association of differential β‐catenin expression with Oct‐4 and Nanog in oral squamous cell carcinoma and their correlation with clinicopathological factors and prognosis

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