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Expression data from breast cancer cells overexpressing NF1-C2

ABSTRACT: NF1-C2 suppresses tumorigenesis and epithelial-to-mesenchymal transition by repressing FoxF1. We used microarray to identify direct targets for NF1-C2.

ORGANISM(S): Homo sapiens

PROVIDER: GSE17636 | GEO | 2010/02/27

SECONDARY ACCESSION(S): PRJNA118575

REPOSITORIES: GEO

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Expression data from breast cancer cells overexpressing NF1-C2

Project description:NF1-C2 suppresses tumorigenesis and epithelial-to-mesenchymal transition by repressing FoxF1. We used microarray to identify direct targets for NF1-C2. The human breast tumor cell line MDA-MB-436 were stably transfected with an expression plasmid including NF1-C2. RNA from these cells and wildtype cells were extracted and hybridized on Affymetrix microarrays (platform GPL570). Three replicates each.

2010-03-09 | E-GEOD-17636 | biostudies-arrayexpress

Expression data from mammary epithelial HC11 cells stably transfected with NF1-C2 or FoxF1

Project description:NF1-C2 suppresses tumorigenesis and epithelial-to-mesenchymal transition by repressing FoxF1. Forkhead Box F1 promotes breast cancer cell migration by upregulating lysyl oxidase and suppressing Smad2/3 signaling

2016-02-04 | GSE77551 | GEO

Expression data from breast cancer cells overexpressing NF1-C2

Project description: Not available

| S-ECPF-GEOD-17636 | biostudies-other

Molecular dissection of somatic NF1 pseudarthrosis

Project description:Neurofibromatosis Type 1 (NF1) is a tumor predisposition syndrome with pleiotropic somatic manifestations, including formation of bone pseudarthrosis after fracture. The pathogenesis of NF1 pseudarthroses remains unclear, though defects in osteogenesis have been posited. Here, we applied time-series single-cell RNA-sequencing (scRNAseq) to patient-matched control and pseudarthrosis-derived primary bone mesenchymal stromal cells (MSCs). We show that osteogenesis occurs in NF1-/- MSCs. In contrast, expression of genetic pathways associated with skeletal mineralization were reduced in NF1-/- cells compared to co-cultured NF1+/- fracture-derived cells.

2022-12-13 | GSE196652 | GEO

Nf1 Deficiency Increases Mammary Collagen Deposition and Restricts Adipocyte Differentiation Before Tumor Formation

Project description:BACKGROUND: The NF1 tumor suppressor gene is the main negative regulator of the RAS pathway and is frequently mutated in various cancers. Women with Neurofibromatosis Type I (NF1) – a tumor predisposition syndrome caused by a germline NF1 mutation – have an increased risk of developing aggressive breast cancer with poorer prognosis. The mechanisms by which NF1 mutation leads to breast cancer tumorigenesis are not well understood. Therefore, the objective of this work was to identify stromal alterations before tumor formation that result in the increased risk and poorer outcome seen among NF1 patients with breast cancer. METHODS: To accurately model the germline monoallelic NF1 mutations in NF1 patients, we utilized an Nf1-deficient rat model with accelerated mammary development and develops highly penetrant breast cancer. RESULTS: We identified increased collagen content in Nf1-deficient rat mammary glands before tumor formation that correlated with age of tumor onset. Additionally, gene expression analysis revealed that Nf1-deficient rat mammary mature adipocytes have increased collagen expression and shifted to a fibroblast and preadipocyte expression profile. This alteration in lineage commitment was also observed with in vitro differentiation but flow cytometry analysis did not show a change mammary adipose-derived mesenchymal stem cell abundance. CONCLUSION: Collectively, these studies uncovered the previously undescribed role of Nf1 in mammary collagen deposition and regulating adipocyte differentiation. In addition to unraveling the mechanism of tumor formation, further investigation of adipocytes and collagen modifications in preneoplastic mammary gland will create a foundation for developing early detection strategies of breast cancer among NF1 patients.

2023-05-08 | GSE231603 | GEO

Transcription profiling of human NF1 heterozygous (NF1+/-) melanocytes from a Neurofibromatosis type 1 patient and NF1 wild type (NF1+/+) melanocytes of a healthy control patient

Project description:One of the major primary features of the neurocutaneous genetic disorder Neurofibromatosis type 1 are the hyperpigmentary café-au-lait macules where dysregulation of melanocyte development, proliferation and differentiation is considered to play a key etiopathogenic role. To gain better insight in the possible role of the tumor suppressor gene NF1, a transcriptomic microarray analysis was performed on human NF1 heterozygous (NF1+/-) melanocytes of a Neurofibromatosis type 1 patient and NF1 wild type (NF1+/+) melanocytes of a healthy control patient, both cultured from normally pigmented and hyperpigmented lesional café-au-lait skin. Out of 13,850 unique genes, a total of 137 had a significant twofold or more up- (72) or down-regulated (65) expression in NF1+/- melanocytes compared to NF1+/+ melanocytes (genotype effect). Considering possible intrinsic genetic variation in lesional skin, melanocytes showed a total of 51 genes having a significant twofold or more up- (37) or down-regulated (14) expression when they were cultured from hyperpigmentary café-au-lait skin compared to normally pigmented skin (lesional skin type effect). NF1+/- café-au-lait skin melanocytes showed 468 genes with a significant two-fold or more up- (183) or down-regulated (285) expression going beyond the sum of the separate main effects (interaction). Detailed analysis enabled the identification of several modulated genes in NF1+/- (café-au-lait skin) melanocytes, mainly involved in controlling cell proliferation and cell maintenance, in cell adhesion and, surprisingly, in the immune response. An interesting finding was that a high number of transcription factor genes were differentially modulated, among which a specific subset - important in melanocyte-lineage development - showed downregulation in a transcriptional cis-regulatory network governing the activation of the melanocyte-specific dopachrome tautomerase (DCT) gene.

2005-02-05 | E-MEXP-258 | biostudies-arrayexpress

Project description:C2 Genome sequencing

| PRJNA680231 | ENA

Coxiella burnetii C2 strain:C2

Project description:Coxiella burnetii C2 strain:C2 Genome sequencing

| PRJNA197120 | ENA

Enterobacter sp. C2 strain:C2

Project description:Enterobacter sp. C2 strain:C2 Genome sequencing

| PRJNA755158 | ENA

Genome-wide gene expression analysis of neurofibroma-derived NF1+/- and NF1-/- Schwann cells

Project description:Analysis of the effect of NF1 second hit mutation to the reading of the whole human genome by comparing the gene expression profiles of neurofibroma derived Schwann cell cultures representing two different NF1 genotypes (NF1+/- and NF1-/-).

2016-12-22 | GSE32029 | GEO

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