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ROS control in human iPS cells reveals early events in spontaneous carcinogenesis

ABSTRACT: ROS control in human iPS cells reveals early events in spontaneous carcinogenesis

PROVIDER: PRJNA508743 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR8285646_1.fastq.gz	Fastqsanger.gz
	SRR8285646_2.fastq.gz	Fastqsanger.gz
	SRR8285648_1.fastq.gz	Fastqsanger.gz
	SRR8285648_2.fastq.gz	Fastqsanger.gz

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ROS control in human iPS cells reveals early events in spontaneous carcinogenesis

Project description:We developed a system to control the intracellular level of reactive oxygen species (ROS) in human iPS cells. By introducing a specific substitution (I69E) into the SDHC protein, a component of the mitochondrial respiratory chain complex, the intracellular ROS level considerably increased. This caused an abnormal development of iPS cells, and these abnormalities were reverted by the overproduction of mitochondria-targeted catalase. When ROS-overproducing iPS cells (ChiPSC12-M cells) were used for subcutaneous inoculation on the backs of nude mice, the mice exhibited tumor formation. The expression of tumor-related FOXC1 transcription factor increased as early as 4 h after the the development of ROS-overproducing iPS cells was initiated. An RNA-seq analysis revealed that 27 transcript clusters among the more than 20,000 transcrips that were examined were highly expressed at 4 h after the initiation of tumor development in ChiPSC12-M cells. Some of these overexpressed transcripts might make networks to activate protooncogenes for spontaneous carcinogenesis.

2021-12-01 | GSE123428 | GEO

Circulating miRNA profile of MMTV-NeuT mouse model of spontaneous mammary carcinogenesis.

Project description:We investigated, in a spontaneous mouse model of breast carcinogenesis (MMTV/NeuT), the modifications in the level of circulating miRNAs during different stages of disease, from early dysplastic stage to overt carcinoma, and their correlation with the pathological stage of the primary mammary lesions.

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Role of endogenous type I Interferon in spontaneous, Her2/Neu oncogene-driven carcinogenesis

Project description:Type I Interferons (IFN-I) are anti-viral and immuno-modulating cytokines involved in many steps across tumor initiation and progression. IFN-I act directly on tumor cells inhibiting cell growth and indirectly by activating immune cells to mount antitumor response. To understand the role of endogenous IFN-I in spontaneous, oncogene-driven carcinogenesis, we characterized tumors arising in Her2/neu transgenic (neuT) mice carrying a non-functional mutation in the IFN-I receptor (IFNAR1), thus being unresponsive to this family of cytokines. Compared to parental neu+/-mice (neuT mice), IFNAR1-/- neu+/- mice (IFNAR-neuT mice) showed earlier onset and increased tumor multiplicity with marked vascularization. Of note, IFNAR-neuT tumors specifically exhibited deregulation of genes having adverse prognostic value in breast cancer patients, including breast cancer stem cells (BCSC) marker aldehyde dehydrogenase-1A1 (ALDH1A1). An increased amount of BCSC was observed in IFNAR-neuT tumors, as assessed by ALDH1A1 enzymatic activity, clonogenic assay and tumorigenic capacity. In vitro exposure of neuT+ mammospheres and cell lines to anti-IFN-I antibodies resulted in increased frequency of ALDH+ cells, suggesting that IFN-I control stemness in tumor cells. Altogether, these results reveal an essential role of IFN-I in NeuT-driven spontaneous carcinogenesis through intrinsic control of BCSC.

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Circulating miRNA profile of MMTV-NeuT mouse model of spontaneous mammary carcinogenesis.

Project description:Circulating miRNA profile of MMTV-NeuT mouse model of spontaneous mammary carcinogenesis.

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Gene expression profile of bone marrow from MMTV-NeuT mouse model of spontaneous mammary carcinogenesis.

Project description:We investigated, in a spontaneous mouse model of breast carcinogenesis (MMTV/NeuT), the modifications in the hematopoietic and stromal bone marrow (BM) compartments and their correlation with the pathological stage of the primary mammary lesions, following the idea that signs of the cross-talk between the BM and elements located in the tumor microenvironment, either neoplastic or stroma/immune cells, can be identified in the very early phases of cancer development, and lead to the instruction of a tumor-promoting hematopoiesis.

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Role of endogenous type I Interferon in spontaneous, Her2/Neu oncogene-driven carcinogenesis

Project description:Role of endogenous type I Interferon in spontaneous, Her2/Neu oncogene-driven carcinogenesis

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Project description:Spinal Muscular Atrophy (SMA) is an autosomal recessive motor neuron disease and is the second most common genetic disorder leading to death in childhood. Motoneurons derived from induced pluripotent stem cells (iPSC) obtained by reprogramming SMA patient and his healthy father fibroblasts, and genetically corrected SMA-iPSC obtained converting SMN2 into SMN1 with target gene correction (TGC), were used to study gene expression and splicing events linked to pathogenetic mechanisms. Microarray technology was used to assess the global gene expression profile as well as splicing events of iPS-derived motorneurons from SMA patient, unaffected father and TGC-treated cells.

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Gene expression profile of bone marrow from MMTV-NeuT mouse model of spontaneous mammary carcinogenesis.

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Global gene expression profile and splicing events of iPS-derived motorneurons from SMA patient, unaffected father and TGC-treated cells

2013-01-04 | E-GEOD-27205 | biostudies-arrayexpress

Early Events in Hematopoietic Cells Reprogramming into iPS Cells

Project description:Fibroblasts are the most commonly used model in probing the complex process of somatic reprogramming. Although hematopoietic cells represents a more convenient and accesible/ or “an excellent alternative” starting cell type, the molecular mechanisms in hematopoietic reprogramming are poorly defined. In the present study, we showed that hematopoietic stem and progenitor cells (HSPCs) with long term repopulating potential, among several HSPC populations, are more amenable for reprogramming, and exhibit an efficient induction of transcriptional program involved in the promation of cell prolifieration and inhibition of apoptosis. In sharp comparison with fibroblasts, HSPCs possess distinct requirements for the activation of Tgf-b and wnt pathways in the initiation phase of reprograming, which can be attributable, at lease partially, to differentiall expression of key signaling genes in these two cell types. Our data demonstrate that lineage and developmental/differentiation stage-specific context define key early events in the reprogramming of hematopoietic cells to pluripotency. Examine the differential global gene expression among different hematopietic cells in reprogramming. LT-HSC, ST-HSC, MP and fibroblasts were used in this study. Doxcycline addition could induce expression of oct4, sox2, klf4 and c-myc, consequently reprogramming these cells into iPS cells. Hematopietic cells cultured with doxcycline for 0, 2, 4 days were sampled, and samples at the same timepoint without doxcycline were also taken to exclude vast gene expression change in hematopoietic cell in-vitro culture. Fibroblast samples induced by doxcycline for 0, 2, 4 days were also introduced to provide comparism between lineages.

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