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Experiment 2: Klf2a, Klf2b and FoxD3 overexpression experiments at 30% epiboly MZspg and WT embryos with or without protein synthesis inhibition

ABSTRACT: Overexpression experiments with or without protein synthesis inhibition were performed to investigate transcriptional targets of Klf2a, Klf2b and FoxD3 in the blastula stage embryos (4,7 hours postfertilization) of wild type or MZspg backgroumd

ORGANISM(S): Danio rerio

PROVIDER: GSE45010 | GEO | 2013/12/31

SECONDARY ACCESSION(S): PRJNA192828

REPOSITORIES: GEO

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Experiment 1: Overexpression experiments at 30% epiboly MZspg and WT embryos with or without protein synthesis inhibition

2013-12-31 | GSE44982 | GEO

Experiment 2: Klf2a, Klf2b and FoxD3 overexpression experiments at 30% epiboly MZspg and WT embryos with or without protein synthesis inhibition

Project description:Overexpression experiments with or without protein synthesis inhibition were performed to investigate transcriptional targets of Klf2a, Klf2b and FoxD3 in the blastula stage embryos (4,7 hours postfertilization) of wild type or MZspg backgroumd Experiments were performed in biological duplicates. Cy3 and Cy5 channels were splitted in Genedata Analyst software, quantile normalised and used for independent comparisons.

2013-12-31 | E-GEOD-45010 | biostudies-arrayexpress

Experiment 1: Overexpression experiments at 30% epiboly MZspg and WT embryos with or without protein synthesis inhibition

Project description:Overexpression experiments with or without protein synthesis inhibition were performed to investigate transcriptional targets of Klf4, FoxD3, and Nanog-like in the blastula stage embryos (4.7 hours postfertilization) of wild type or MZspg background. Experiments were performed in biological triplicates. Cy3 and Cy5 channels were splitted in Genedata Expressionist and Analyst software, quantile normalised and used for independent comparisons.

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Experiment 4: Klf4, FoxD3, FoxD5 and combined FoxD3 and FoxD5 loss-of-function experiments at 30% epiboly Wild Type zebrafish embryos

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Experiment 4: Klf4, FoxD3, FoxD5 and combined FoxD3 and FoxD5 loss-of-function experiments at 30% epiboly Wild Type zebrafish embryos

Project description:Morpholino injections were performed to investigate transcriptional targets of Klf4, FoxD3 and FoxD5 in the blastula stage embryos (4,7 hours postfertilization) of wild type zebrafish embryos. Experiments were performed in biological duplicates or triplicates. Cy3 and Cy5 channels were splitted in Genedata Analyst software, quantile normalised and used for independent comparisons.

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Experiment 3: Klf2a and Klf2b loss-of-function experiments at 30% epiboly Wild Type zebrafish embryos

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Experiment 3: Klf2a and Klf2b loss-of-function experiments at 30% epiboly Wild Type zebrafish embryos

Project description:Morpholino injections were performed to investigate transcriptional targets of Klf2a, and Klf2b in the blastula stage embryos (4,7 hours postfertilization) of wild type zebrafish embryos. Experiments were performed in biological duplicates. Cy3 and Cy5 channels were splitted in Genedata Analyst software, quantile normalised and used for independent comparisons.

2013-12-31 | E-GEOD-45011 | biostudies-arrayexpress

Characterization of FOXD3 cofactors by BioID

Project description:FOXD3 is essential in embryonic stem cells, however the primary molecular mechanism is unclear. Here, we performed BioID to identify proteins collaborating with FOXD3 in protecting embryonic stem cell survival.

2023-05-08 | PXD035284 | Pride

FOXD3 is a novel tumor suppressor in lung cancer

Project description:The transcription factor forkhead box D3 (FoxD3) is a transcriptional factor which belongs to forkhead box (Fox) transcription factor family. The functions of FOXD3 in embryogenesis and in the development of neural crest cells have been clearly defined. Its tumor suppressor function hasbeen found in many types of cancer in recent years. However, the study about its roles in lung cancerdevelopment is still lacking. Our study found that deficiency of FoxD3 in lung cancer enhanced cell growth and cell invasion. RNA-sequence analysis demonstrated that loss of FoxD3 mainly affected cell cycle progression related gene expression. Knockdown of FoxD3 led to G2-M cell accumulation with up-regulation of DNA replication licensing factor MCM5 and MCM4 as well as cell cycle regulator polo-like kinase-1 (PLK1) and CDC6. Over-expression of those genesin lung cancer was associated with poor clinical outcomes of lung cancer patients. We also identified high mobility group box-1(HMGB1), Hras and Ephrin B1 gene expression increase after FoxD3 silencing which may participate in enhanced lung cancer cell invasion. Our study identifiedtumor suppressor function of FoxD3 in lung cancer andwe did the first comprehensive analysis of the genes regulated by FoxD3 for cell proliferation and invasion in lung cancer. The identified genes regulated by FoxD3 through our analysis will provide valuable information to uncover the mechanism of FoxD3 tumor suppressor function.

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Genome-wide maps of chromatin binding of FOXD3

Project description:The tumor-initiating cells (TIC) are cell population that can initiate tumor, mediate drug resistance, and give rise to metastasis. FOXD3 is a forkhead box (Fox) transcription factor family that regulates the pluripotency of embryonic stem cell and tumorigenicity. However, it is unclear whether FOXD3 play any role in TIC and tumor metastasis. Here, we report that FOXD3 is down-regulated in tumor initiating cells and negatively correlated with higher histologic grades and positive lymph node metastasis. FOXD3 repress TIC expansion, cell migration, drug resistance and osteogenesis in vitro and in vivo. Mechanically, we found that FOXD3 repress a cohort of genes including SET and WDR5 and to regulate several TIC related signaling pathway. Moreover, SET and WDR5 was positively correlated with the CSC abundance and tumor progression. Besides, patients with high expression of SET and WDR5 presented a poorer overall survival. Collectively, our work defined that FOXD3-WDR5-SET axis that repress TIC accumulation and lung cancer progression.

2017-01-10 | GSE93323 | GEO

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