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Characterization of cell cycle phase specific chromatin accessibility using ATAC seq after FOXD3 depletion

ABSTRACT: Characterization of cell cycle phase specific chromatin accessibility using ATAC seq after FOXD3 depletion

PROVIDER: PRJNA760538 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15715568_1.fastq.gz	Fastqsanger.gz
	SRR15715568_2.fastq.gz	Fastqsanger.gz
	SRR15715569_1.fastq.gz	Fastqsanger.gz
	SRR15715569_2.fastq.gz	Fastqsanger.gz
	SRR15715570_1.fastq.gz	Fastqsanger.gz

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Characterization of cell cycle phase specific chromatin accessibility using ATAC seq after FOXD3 depletion

Project description:We performed ATAC seq of inducible FOXD3 KO cells after cell cycle phase sorting to determine impact of FOXD3 loss on chromatin accessibility.

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Characterization of active chromatin marks by CUT&Tag after FOXD3 depletion

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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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Characterization of active chromatin marks by CUT&Tag after FOXD3 depletion

Project description:Characterization of active chromatin marks by CUT&Tag after FOXD3 depletion

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Characterization of FOXD3 cofactors by BioID

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Project description:In this study, we demonstrated that FOXD3, acting as a repressor in the expansion of lung cancer TICs, was negatively correlated with histological grades and metastasis in lung cancer, and provided evidence that FOXD3 repressed the TIC expansion, cell invasion and drug resistance in vivo and in vitro. Global genomic RNA-Seq and Chip-seq analyses identified WDR5 and SET as the direct targets of FOXD3 in lung cancer. Inhibition of WDR5 and SET could partially rescue TIC abundance, cell invasion, osteogenesis, and gene expression signature upon depletion of FOXD3. Clinically, we revealed that FOXD3 was negatively correlated with WDR5 and SET expression, CSC abundance, and prognosis of lung cancer.

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