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NANOG metabolically reprograms tumor-initiating stem-like cells in oxidative phosphorylation and fatty acid metabolism

ABSTRACT: Stem cell markers such as NANOG have been implicated in various cancers; however, the functional contribution of NANOG to cancer pathogenesis has remained unclear. In the present study, we show that Toll-like receptor 4 (TLR4) signaling phosphorylates E2F1 to transactivate NANOG. Down-regulation of Nanog significantly reduces tumor development. In the search for the NANOG-dependent mechanisms underlying growth of tumor-initiating stem-like cells (TICs), NANOG ChIP-seq identifies the genes associated with mitochondrial metabolic pathways.

ORGANISM(S): Mus musculus

PROVIDER: GSE68237 | GEO | 2016/01/07

SECONDARY ACCESSION(S): PRJNA282110

REPOSITORIES: GEO

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NANOG metabolically reprograms tumor-initiating stem-like cells in oxidative phosphorylation and fatty acid metabolism

Project description:Stem cell markers such as NANOG have been implicated in various cancers; however, the functional contribution of NANOG to cancer pathogenesis has remained unclear. In the present study, we show that Toll-like receptor 4 (TLR4) signaling phosphorylates E2F1 to transactivate NANOG. Down-regulation of Nanog significantly reduces tumor development. In the search for the NANOG-dependent mechanisms underlying growth of tumor-initiating stem-like cells (TICs), NANOG ChIP-seq identifies the genes associated with mitochondrial metabolic pathways. Genome wide Identification of Nanog binding partners in tumor initating stem cells

2016-01-07 | E-GEOD-68237 | biostudies-arrayexpress

NANOG Metabolically Reprograms Tumor-Initiating Stem-like Cells through Tumorigenic Changes in Oxidative Phosphorylation and Fatty Acid Metabolism.

Project description: Not available

| S-EPMC4715587 | biostudies-literature

Circular RNA expression profile in mitochondria fractions of liver tumour-initiating cells

Project description:Tumour-initiating cells (TICs), also termed as cancer stem cells, contribute to tumour initiation, metastasis, progression and drug resistance. Metabolic reprogramming is a cancer hallmark and plays vital roles in liver tumorigenesis. However, the role of metabolic reprogramming in TICs remains poorly explored.Here we isolated mitochondria from liver TICs and non-TICs, and detected the expression levels of mitochondrial encoded circRNAs in TICs and non-TICs.

2023-01-25 | GSE223661 | GEO

Targeting Unique Metabolic Properties of Breast Tumor Initiating Cells

Project description:Bulk cancer cell populations are known to display distinct metabolic properties compared to their normal counterparts. However, relatively little is known about heterogeneity of metabolic properties within tumors. In this study we show that, analogous to some normal stem cells, breast tumor initiating cells (TICs, also called cancer stem cells) have distinct metabolic properties compared to non-tumorigenic cancer cells (NTCs). Transcriptome profiling using RNA-Seq revealed TICs under-express genes involved in mitochondrial oxidative phosphorylation and although TICs are relatively quiescent, they preferentially perform glycolysis over oxidative phosphorylation compared to NTCs. TICs contain fewer mitochondria and display lower expression and activity of pyruvate dehydrogenase (Pdh), a key regulator of oxidative phosphorylation. Metabolic reprogramming of TICs by pharmacologic activation of Pdh preferentially eliminates TICs in vitro and in vivo. Our findings reveal unique metabolic properties of TICs and indicate that metabolic reprogramming represents a promising strategy for targeting these cells.

2014-07-31 | GSE41286 | GEO

Targeting Unique Metabolic Properties of Breast Tumor Initiating Cells

2014-07-31 | E-GEOD-41286 | biostudies-arrayexpress

Mitocans target tryptophan metabolism to remove the mimicry of tumour-initiating cells

Project description:Following therapy, tumour-initiating cells (TICs) survive and give rise to second-line tumours. Gene set enrichment analysis of microarray data and microRNA analysis confirmed the validity of spheroid cultures as models of TICs for breast and prostate cancer and mesothelioma cell lines. Pathway analysis revealed increased Trp metabolism in all types of TICs with indoleamine 2,3-dioxygenase (IDO) as the rate-limiting enzyme. TICs also expressed higher levels of the Trp uptake system consisting of CD98 and LAT1 with functional consequences. Mitocans, represented by vitamin E (VE) analogues, suppressed IDO1 in TICs with functional mitochondrial complex II, a target for the agents. IDO1 expression was regulated via a mechanism involving both transcriptional and post-transcriptional mechanisms. IDO1 increase and its suppression by VE analogues were replicated in TICs from primary human glioblastomas. Our work points to Trp metabolism as a novel mechanism of TICs to bypass the immune surveillance and to VE analogues as agents that remove this ‘mimicry’.

2013-11-01 | GSE41980 | GEO

Gene expression signatures for Nanog-positive and Nanog-negative hepatocellular carcinoma cells

Project description:Whole genome microarray expression profiling of HCC cell line (Huh7) and patients derive primary HCC cells (T1115 and T1224) expressing Nanog or not. Results provide insight into the role of Nanog in transcriptional regulation.

2014-11-13 | GSE33741 | GEO

Mitocans target tryptophan metabolism to remove the mimicry of tumour-initiating cells

2013-11-01 | E-GEOD-41980 | biostudies-arrayexpress

Nanog-induced intestinal and colonic hyperplasia

Project description:Though expression of the homeobox transcription factor Nanog is generally restricted to pluripotent cells and early germ cells, recent reports have found that Nanog is re-expressed in somatic and germ cell tumors associated with poor differentiation and aggressive disease progression. To elucidate its oncogenic properties, a modified Tet-On system was utilised to generate Nanog-inducible mice. By dexamethasone and doxycycline injection, similar Nanog expression levels as in wild-type embryonic stem cells were obtained in all major organs except for brain. Ectopic Nanog expression resulted in intestinal and colonic epithelium hyperplasia-intestinal villi had doubled in length and hyperplastic epithelium outgrowths were seen after 7 days. The tumor suppressor gene Cdx2 was downregulated at onset of Nanog expression, suggesting that crosstalk between Nanog and Cdx2 is conserved from early embryo development to adulthood. Although the mice died before they could form tumors, Cdx2 repression and intestinal hyperplasia links Nanog to tumor initiation.

2014-08-11 | GSE31413 | GEO

Nanog-induced intestinal and colonic hyperplasia

2014-08-11 | E-GEOD-31413 | biostudies-arrayexpress

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