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Transcriptome datasets of the Quaking (QKI) gene knock-down human oral squamous cell carcinoma (OSCC) cells

ABSTRACT: Transcriptome datasets of the Quaking (QKI) gene knock-down human oral squamous cell carcinoma (OSCC) cells

PROVIDER: PRJNA647335 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12267305_1.fastq.gz	Fastqsanger.gz
	SRR12267305_2.fastq.gz	Fastqsanger.gz
	SRR12267306_1.fastq.gz	Fastqsanger.gz
	SRR12267306_2.fastq.gz	Fastqsanger.gz
	SRR12267307_1.fastq.gz	Fastqsanger.gz

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Transcriptome datasets of the Quaking (QKI) gene knock-down human oral squamous cell carcinoma (OSCC) cells

Project description:Here, we elucidated whether miR-200 family members control RNA-binding protein quaking (QKI), a newly identified tumor suppressor that is regulated during EMT. QKI expression was suppressed by miR-200 overexpression, and the 3'-UTR of QKI mRNA was directly targeted by miR-200 in luciferase reporter assays. ShRNA-mediated knockdown of QKI led to pronounced EMT and protumor effects in both in vitro and in vivo studies of oral squamous cell carcinoma. Furthermore, high expression of QKI protein is associated with favorable prognosis in surgically resected head and neck squamous cell carcinoma and lung adenocarcinoma. In conclusion, QKI increases during EMT and is targeted by miR-200; while, it suppresses EMT and tumorigenesis. We suggest that QKI and miR-200 form a negative feedback loop to maintain homeostatic responses to EMT-inducing signals.

2020-07-21 | GSE154730 | GEO

QKI and miR-155 in inflammation and leukemogenesis

Project description:Transcription profiling by array of siRNA against Quaking (QKI) transcripts to identify transcripts that are modulated by QKI activity. MiR-155 is an oncogene and we report here that it targets QKI transcripts. Therefore, we believe that QKI acts as a tumor suppressor gene in different leukemias. We ablated the expression of QKI transcripts using siRNAs in order to further elucidate the effects of QKI in leukemogenesis, and how miR-155 and QKI functionally interact with each other.

2016-01-17 | E-MTAB-2375 | biostudies-arrayexpress

Transcriptome-wide HITS-CLIP of Quaking (QKI) in TGF-Beta-treated HMLE (Mesenchymal-like) cells

Project description:Members of the miR-200 family are critical gatekeepers of the epithelial state, restraining expression of pro-mesenchymal genes that drive epithelial-mesenchymal transition (EMT) and contribute to metastatic cancer progression. Here, we show that miR-200c and another epithelial-enriched miRNA, miR-375, exert widespread control of alternative splicing in cancer cells. This is achieved by their strong suppression of the RNA binding protein Quaking (QKI), which is required to mediate the splicing changes regulated by these miRNAs. During EMT, QKI-5 directly binds to and regulates hundreds of alternative splicing events and exerts pleiotropic effects, such as increasing cell migration and invasion and restraining tumour growth, without appreciably affecting mRNA levels. QKI-5 is both necessary and sufficient to direct EMT alternative splicing changes, and this splicing signature is broadly conserved across many epithelial-derived cancer types. Importantly, several actin cytoskeleton-associated genes are directly targeted both by QKI and miR-200c, revealing coordinated control of alternative splicing and mRNA abundance during EMT. These findings demonstrate the existence of a miR-200/miR-375/QKI axis that impacts cancer-associated epithelial cell plasticity through widespread control of alternative splicing. The purpose of the CLIP experiment was to determine direct targets of QKI.

2018-03-15 | GSE111188 | GEO

Transcriptome-wide identification of RNA-binding protein and microRNA target sites by PAR-CLIP: QKI data

Project description:To assess whether the transcripts identified by PAR-CLIP are regulated by the RNA-binding protein (RBP) Quaking (QKI), we analyzed the mRNA levels of mock-transfected and QKI-specific siRNA-transfected cells with microarrays. Transcripts crosslinked to QKI were significantly upregulated upon siRNA transfection, indicating that QKI negatively regulates bound mRNAs (Figure 3H of PMID 20371350), consistent with previous reports of QKI being a repressor. The RBP QKI was depleted by siRNAs and the expression level was compared to mock-transfected HEK 293 cells.

2010-05-27 | E-GEOD-21574 | biostudies-arrayexpress

Transcriptome-wide regulation of pre-mRNA splicing and expression by the RNA-binding protein Quaking during monocyte to macrophage differentiation [RNA-Seq]

Project description:Expression levels of the RNA-binding protein Quaking (QKI) are low in monocytes of early, human atherosclerotic lesions, but abundant in macrophages of advanced plaques. Specific depletion of QKI protein impaired monocyte adhesion, migration, differentiation into macrophages, and foam cell formation in vitro and in vivo. RNA-seq and microarray analysis of human monocyte and macrophage transcriptomes, including those of a unique QKI haploinsufficient patient, revealed striking changes in QKI-dependent mRNA levels and splicing of RNA transcripts. RNA-seq analysis of primary monocytes and macrophages from a QKI haploinsufficient patient and their (control) sibling.

2016-01-04 | E-GEOD-74978 | biostudies-arrayexpress

Transcriptome-wide identification of RNA-binding protein and microRNA target sites by PAR-CLIP: QKI data

2010-04-29 | GSE21574 | GEO

Transcriptome-wide regulation of pre-mRNA splicing and expression by the RNA-binding protein Quaking during monocyte to macrophage differentiation [Microarray]

Project description:Expression levels of the RNA-binding protein Quaking (QKI) are low in monocytes of early, human atherosclerotic lesions, but abundant in macrophages of advanced plaques. Specific depletion of QKI protein impaired monocyte adhesion, migration, differentiation into macrophages, and foam cell formation in vitro and in vivo. RNA-seq and microarray analysis of human monocyte and macrophage transcriptomes, including those of a unique QKI haploinsufficient patient, revealed striking changes in QKI-dependent mRNA levels and splicing of RNA transcripts. Microarray analysis of gene expression and splicing in THP-1 cells transfected with shRNAs, with or without PMA treatment to induce differentiation. 12 total samples were analyzed: THP-1 monocytic cell line transfected with QKI or control shRNAs; samples taken at day 0 or day 3 of PMA-induced differentiation into macrophages.

2016-01-04 | E-GEOD-74887 | biostudies-arrayexpress

RNAi knock down of QKI in human astrocyte glioma cells shows that QKI depletion affects expression of immune response-related genes

Project description:We studied the effect of small interfering RNA (siRNA)-mediated QKI depletion on global gene expression in human oligodendroglioma cells and astrocyte glioma cells

2009-08-18 | E-MEXP-1393 | biostudies-arrayexpress

Transcriptome-wide regulation of pre-mRNA splicing and expression by the RNA-binding protein Quaking during monocyte to macrophage differentiation [RNA-Seq]

2016-01-04 | GSE74978 | GEO

Transcriptome-wide regulation of pre-mRNA splicing and expression by the RNA-binding protein Quaking during monocyte to macrophage differentiation [Microarray]

Project description:Expression levels of the RNA-binding protein Quaking (QKI) are low in monocytes of early, human atherosclerotic lesions, but abundant in macrophages of advanced plaques. Specific depletion of QKI protein impaired monocyte adhesion, migration, differentiation into macrophages, and foam cell formation in vitro and in vivo. RNA-seq and microarray analysis of human monocyte and macrophage transcriptomes, including those of a unique QKI haploinsufficient patient, revealed striking changes in QKI-dependent mRNA levels and splicing of RNA transcripts. Microarray analysis of gene expression and splicing in THP-1 cells transfected with shRNAs, with or without PMA treatment to induce differentiation.

2016-01-04 | GSE74887 | GEO

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