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Effect of SUFU overexpression and knockdown on gene expression profile in breast cancer epithelial cells

ABSTRACT: Effect of SUFU overexpression and knockdown on gene expression profile in breast cancer epithelial cells

PROVIDER: PRJNA780414 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16946492_1.fastq.gz	Fastqsanger.gz
	SRR16946492_2.fastq.gz	Fastqsanger.gz
	SRR16946493_1.fastq.gz	Fastqsanger.gz
	SRR16946493_2.fastq.gz	Fastqsanger.gz
	SRR16946494_1.fastq.gz	Fastqsanger.gz

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Effect of SUFU overexpression and knockdown on gene expression profile in breast cancer epithelial cells

Project description:SUFU is a negative regulator of the hedgehog signaling pathway and its abnormal expression has been found in several human cancers, whereas the role of SUFU in the malignant development of breast cancer has not been fully elucidated. We performed RNA-seq to determine the impact of SUFU overexpression and knockdown on global gene expression profile in SKBR3 and HCC1954 cells. Our results show that sufu affects ferroptosis phenotype via modulating yap-dependent ACSL4 in breast cancer cells.

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Sufu and Spop cooperate to suppress SHH medulloblastoma tumorigenesis via regulation of Gli2 protein stability [ChIP-seq]

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Project description:CS sufu Raw sequence reads

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BS sufu

Project description:BS sufu Raw sequence reads

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RNA Sequencing of postnatal mouse Math1-Cre; Sufu flox/- cerebellum

Project description:Transcriptional profiling to identify genes differentially regulated by Sufu during cerebellum development. Sufu was specifically deleted from the granule neuron compartment using Math1-driven Cre recombinase.

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Project description:Sepsis is a potentially life-threatening condition caused by the body's response to a severe infection. However, the pathogenesis of sepsis remains unclear. Here, we found that Suppressor of Fused (Sufu), a classical negative regulator of Hedgehog signaling, is downregulated in patients with sepsis and in murine peritoneal macrophages treated with lipopolysaccharide (LPS). Deletion of Sufu aggravated LPS-induced lung injury and lethality in mice, and augmented LPS induced proinflammatory gene expression in cultured macrophages. By RNA-seq transcriptome profiling, we identified Sufu as a negative regulator of the TLR-triggered inflammatory response.

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Gene expression profiles induced by knockdown and overexpression of p63 variants in MCF-10A mammary epithelial cell line

Project description:p63 is critical for epithelial development yet little is known about the transcriptional programmes it regulates. The p63 transactivating (TA) isoforms contain an amino-terminal exon that encodes a p53-like transactivation domain, whereas ÎN-isoforms lack this domain but contain the common DNA binding domain (DBD), suggesting that TAp63 and ÎNp63 isoforms may have opposing functions. By characterising transcriptional changes and cellular effects following modulation of p63 expression, we have defined a vital role for p63 in cellular adhesion. Knockdown of p63 expression caused downregulation of cell adhesion-associated genes, cell detachment and anoikis in mammary epithelial cells and keratinocytes. Conversely, overexpression of the TAp63Î³ or ÎNp63Î± isoforms of p63 upregulated cell adhesion molecules, increased cellular adhesion and conferred resistance to anoikis. Total RNA was isolated 48 h after retroviral or adenoviral infection and was subjected to reverse transcription, labelling and hybridization. The knockdown samples were performed in duplicate with shRNA vector control, shRNA targetting all isoforms of p63 (shDBD) and shRNA targetting p63 isoforms containing the transactivating (TA) domains. The overexpression samples were performed in triplicate with vector control, overexpression of the ÎNp63Î± isoform, and overexpression of the TAp63Î³ isoforms.

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