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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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			Action	DRS
	SRR8291381.fastq.gz	Fastqsanger.gz
	SRR8291382.fastq.gz	Fastqsanger.gz
	SRR8291383.fastq.gz	Fastqsanger.gz
	SRR8291384.fastq.gz	Fastqsanger.gz

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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 gastric cancer MKN-45 cells with or without the overexpression of transcriptional factor SIX2

Project description:Analysis of MKN-45 cells following SIX2 stable overexpression or not. SIX2 regulates various mRNA expression in MKN-45 cells.Results provide insight into the role of SIX2-involved mechanisms underlying SIX2-mediated effects on gastric cancer stemness.

2024-06-09 | GSE234584 | 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.

2019-03-10 | GSE116984 | GEO

Genome-wide maps of chromatin state in MCF-7 cells with six2 overexpression or not

Project description:By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA in MCF-7 cells with six2 overexpression or not, we generated genome-wide chromatin-state maps of these two cells. We identified the detailed binding sites of six2 in MCF-7 cells.

2019-03-10 | GSE117145 | GEO

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

2011-02-01 | GSE26290 | GEO

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.

2018-01-18 | GSE108102 | GEO

High Glucose (HG) treated morula vs control glucose (CTL) treated morula

Project description:Early bovine cleavage (day 0 to 3) was treated with high glucose (5mM) or control glucose (0.2mM) then total day 3 embryos were cultured in control condition until day 5 when gene expression was assessed in developping morula by microarray 4 replicates of 10 morulae/rep was produced for high glucose and control treatment. According to a dye swap design, 4 arrays were used, one array for each comparison between HG and control, i.e replicate 1 from HG were compared to replicate 1 from CTL, rep 2 from HG were compared to rep 2 from CTL, rep 3 HG vs rep 3 CTL, rep 4 HG vs rep 4 CTL.

2012-09-01 | E-GEOD-40521 | biostudies-arrayexpress

Gene expression profiling of Six2-positive nephron progenitors from mouse embryo

Project description:Nephron progenitors in the embryonic kidney propagate while generating differentiated nephrons. However, the progenitors in mice terminally differentiate shortly after birth. We defined culture conditions to selectively propagated nephron progenitors in vitro in an undifferentiated state. To understand how expression profiles of Six2+ cells changed during culture in vitro compared with in vivo, we performed microarray analysis of Six2+ cells at E11.5 (starting material) and P0 (experiencing 8 days in vivo), and cultured Six2+ cells at E11.5 for 8 days or 19 days. Microarray analysis were performed with isolated Six2-positive nephron progenitors from transgenic mice embryo at E11.5 or P0, and cultured E11.5 Six2+ cells for 8 or 19 days in conditioned media. P0 non-progenitors represent Six2-GFP-negative cells at P0.

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

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