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RNA-seq Analysis in 4T07 Control (4T07-CTL) and Six2 Overexpression (4T07-Six2) cells

ABSTRACT: RNA-seq Analysis in 4T07 Control (4T07-CTL) and Six2 Overexpression (4T07-Six2) cells

PROVIDER: PRJNA508930 | ENA |

REPOSITORIES: ENA

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RNA-seq Analysis in 4T07 Control (4T07-CTL) and Six2 Overexpression (4T07-Six2) cells

Project description:To determine the molecular mechanisms by which Six2 regulates metastatic colonization, we performed RNA-seq analysis on murine triple-negative 4T07 Control (4T07-CTL) and Six2 overexpressing (4T07-Six2) cells. Using both targeted and unbiased gene signature analyses, we found that Six2 differentially regulates gene signatures associated with stemness. Additionally, we confirmed that in several triple-negative breast cancer (TNBC) models, Six2 enhanced the expression of genes (identified as among the highest upregulated genes in response to Six2 overexpression) associated with embryonic stem cell programs. When combined with our in vitro and in vivo stemness-associated phenotypic assays, these data suggest that Six2 may play a similar role in mediating stemness characteristics during tumor progression as it does during development, and that this role may allow it to mediate late-stage metastasis by enhancing the ability of cells to self-renew and survive at secondary sites.

2020-01-30 | GSE123489 | GEO

Genome-wide maps in MCF-7 cells with six2 or CYP4Z1 3'UTR or CYP4Z2P 3'UTR overexpression or not

Project description:Analysis of MCF-7 cells following six2 or CYP4Z1 3'UTR or CYP4Z2P 3'UTR overexpression. Overexpression of six2 or CYP4Z1 3'UTR or CYP4Z2P 3'UTR positively regulates the abundance of embryonic stem cell function. Results provide insight into the role of six2 mediated-regulation on the ceRNA network between CYP4Z1 and pseudogene CYP4Z2P in breast cancer stemness.

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Expression data from control and Phospholipid dependent kinase 1 (PDK1) null cytotoxic T-lymphocytes (CTL) and from control and Akt inhibitor treated CTL

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Expression data from control and Phospholipid dependent kinase 1 (PDK1) null cytotoxic T-lymphocytes (CTL) and from control and Akt inhibitor treated CTL

Project description:In cytotoxic T cells (CTL), Protein Kinase B /Akt is activated by the T cell antigen receptor (TCR) and the cytokine Interleukin 2 (IL2), in part by phosophorylation of Akt by Phospholipid dependent kinase 1 (PDK1). The role of PDK1 and Akt in CTL has however not been fully defined. In order to explore the relative roles of these kinases in CTL we used microarrays to profile the gene expression of control and PDK1 null CTL. In separate experiments we compared the gene expression profiles of control and Akt inhibitor treated CTL. CTL were generated from 3 mice each carrying two loxP flanked PDK1 alleles plus a tamoxifen inducible Cre transgene. PDK1 was then deleted from these CTL by tamoxifen treatment and the gene expression pattern determined by microarray. Tamoxifen treated PDK1wt/wt TamoxCre+ CTL generated from 3 PDK1wt/wt TamocCre+ mice were used as a control. In separate experiments CTL were were generated from 3 wild-type mice and then half the CTL generated from each mouse were treated with the Akt inhibitor AktI-1/2. The gene expression patterns of the AktI treated and the untreated CTL were then compared by microarray.

2011-02-01 | E-GEOD-26290 | biostudies-arrayexpress

Exploring Six2 distal enhancer interactome in developing mouse kidney

Project description:The Six2 distal enhancer regulates expression of the 60 kb-downstream gene Six2, but does not regulate the Six3 gene which is 70 kb further downstream. CTCF ChIP-Seq and Hi-C data points to a chromatin domain boundary between Six2 and Six3 which may intervene interaction between Six2-DE and Six3. The irradiation-induced Brachyrrhine (Br) mutant allele was found to carry a 320 kb genomic inversion that includes Six2 and Six3, but not Six2DE. This repositioned Six2 under Six3 enhancer control and Six3 under Six2 distal enhancer control. Consistent with this, Six3 is ectopically expressed in Br/+ kidneys and Six2 expression is reduced. To test whether there is a change of interaction between Six2 distal enhancer and Six2 or Six3 promoters, we performed 4C-Seq in E16.5 wildtyp or Br/+ mice nephron-genic zone cells.

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2016-04-14 | E-GEOD-79024 | biostudies-arrayexpress

Genome-wide maps of Six2 and b-catenin in mesenchymal nephron progenitors

Project description:Self-renewing undifferentiated nephron progenitors express Six2, a transcription factor that is required for their maintenance as undifferentiated progenitors. Differentiation of nephron progenitors is triggered by Wnt/b-catenin signaling. In order to understand how Six2 and Wnt signaling counteract each other, we performed ChIP-seq of Six2 and b-catenin in mesenchymal nephron progenitor cells. Nephron progenitors were FACS-isolated from BAC transgenic Six2GFPcre-positive embryonic kidneys at E16.5. For Six2 ChIP, freshly FACS isolated Six2+ cells were used. For b-catenin ChIP, FACS isolated Six2+ cells were aggregated by centrifugation at 850g for 5min and incubated in 10%FBS/DMEM containing 4uM BIO for 24hrs.

2012-09-11 | E-GEOD-39837 | biostudies-arrayexpress

Transcriptional responses in SIX2 nephron progenitor cells following mitochondrial complex III subunit 7 (Qpc) inactivation

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2022-06-29 | GSE158299 | GEO

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