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Transcriptome of ovarian cancer cells overexpressing SYNCRIP or SNU13

ABSTRACT: Transcriptome of ovarian cancer cells overexpressing SYNCRIP or SNU13

PROVIDER: PRJNA1010739 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25793481_1.fastq.gz	Fastqsanger.gz
	SRR25793481_2.fastq.gz	Fastqsanger.gz
	SRR25793482_1.fastq.gz	Fastqsanger.gz
	SRR25793482_2.fastq.gz	Fastqsanger.gz
	SRR25793483_1.fastq.gz	Fastqsanger.gz

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Transcriptome of ovarian cancer cells overexpressing SYNCRIP or SNU13

Project description:We showed that in response to chemotherapy, dying cancer cells can secrete spliceosomal components into the extracellular space. These therapy-induced secretomes enriched with spliceosomal components promote the chemoresistance of recipient tumor cells. We demonstrated that spliceosomal proteins SNU13 and SYNCRIP can relocalize from dying tumor cells to recipient tumor cells via extracellular vesicles. To investigate whether the increased abundance of splicing factors could be the reason for the acquisition of a more aggressive phenotype by tumor cells, we got SKOV3 cell lines stably overexpressing SYNCRIP or SNU13. These cell lines were more resistant to cisplatin compared to control cell line expressing empty vector. Next, to investigate how the therapy response is formed in tumor cells with and without overexpression of spliceosomal proteins SNU13 or SYNCRIP, we performed RNAseq analysis of these cells before and 24 hours after cisplatin treatment. Enrichement analyses showed that in response to cisplatin, genes associated with DNA repair and cell cycle regulation were upregulated in cancer cell lines overexpressing SYNCRIP or SNU13 compared with control cells. This study revealed previously unknown signaling molecules in the microenvironment of ovarian cancer that have potential clinical significance.

2024-04-24 | GSE241913 | GEO

Comparisons of the global gene profile between CLDN4-overexpressing and CLDN4-silencing ovarian cancer cells.

Project description:A microarray analysis was performed to compare the global gene expression profile between CLDN4-overexpressing (Control) and CLDN4-silencing SKOV-3 ovarian cancer cells.

2010-12-15 | GSE22493 | GEO

Comparisons of the global gene profile between CLDN4-overexpressing and CLDN4-silencing ovarian cancer cells.

Project description:A microarray analysis was performed to compare the global gene expression profile between CLDN4-overexpressing (Control) and CLDN4-silencing SKOV-3 ovarian cancer cells. CLDN4 gene was knocked down by CLDN4 siRNA lentivirus. Total RNA was extracted and microarray was perfomed to compare the gene profiling changes between CLDN4-overexpressing (Control) and CLDN4-silencing cells. The experiment was performed in triplicate.

2010-12-15 | E-GEOD-22493 | biostudies-arrayexpress

Genetically modified ID8 cells to study the role of GBP1 in ovarian cancer

Project description:Genetically modified ovarian cancer cells were used to study the role of GBP1. Proteomics-based thermal stability assay (CETSA) was performed on GBP1 knockdown and overexpressing ID8 ovarian cancer cells. Shotgun proteomics was also performed on these cells.

2024-01-26 | PXD040444 | Pride

Gene expression data of EMT-TFs overexpressing ovarian cancer cell lines

Project description:Gene expression data of EMT-TFs overexpressing ovarian cancer cell lines

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Genome-wide high-throughput sequencing analysis of TLR4-overexpressing ovarian cancer cells treated with taxol and curcumin

Project description:The purpose of this study is to approach overexpression of TLR4 which contributes the drug resistance in ovarian cancer cells. However, curcumin overcomes this effects. Comparison of the transcriptional regulated genes were performed: (1) analysis of TLR4-overexpressing (T4) and mock (MCS) SKOV3 cells by taxol treatment; (2) assay of taxol alone and combined with curcumin treatments in TLR4-overexpressing (T4) SKOV3 cells. Differential expression analysis was performed with ≥ 2-fold or ≤0.5-fold (p<0.05) changed expression for pathway enrichment analysis.

2022-08-02 | GSE135279 | GEO

single cell RNA-seq in transplanted bone marrow cells from SYNCRIP conditional mouse model

Project description:SYNCRIP depletion results in HSCs losing their self renewal abilities. Single cell sequencing was conducted in SYNCRIP WT and KO bone marrow LK (lineage -, cKit+) cells to decipher the effect of Syncrip deletion on cellular identities along the hematopoietic hierarchy, and to gain an in-depth assessment of the transcriptomic changes in different cell types upon SYNCRIP loss.

2023-03-01 | GSE202421 | GEO

The cytoplasmic SYNCRIP mRNA interactome of mammalian neurons

Project description:SYNCRIP, a member of the cellular heterogeneous nuclear ribonucleoprotein (hnRNP) family of RNA binding proteins, regulates various aspects of neuronal development and plasticity. Although SYNCRIP has been identified as a component of cytoplasmic RNA granules in dendrites of mammalian neurons, only little is known about the specific SYNCRIP target mRNAs that mediate its effect on neuronal morphogenesis and function. Here, we present a comprehensive characterization of the cytoplasmic SYNCRIP mRNA interactome using iCLIP in primary rat cortical neurons. We identify hundreds of bona fide SYNCRIP target mRNAs, many of which encode for proteins involved in neurogenesis, neuronal migration and neurite outgrowth. From our analysis, the stabilization of mRNAs encoding for components of the microtubule network, such as doublecortin (Dcx), emerges as a novel mechanism of SYNCRIP function in addition to the previously reported control of actin dynamics. Furthermore, we found that SYNCRIP interacts with miRISC and synergizes with pro-neural miRNAs, such as miR-9. Based on our findings, we propose a model whereby SYNCRIP promotes early neuronal differentiation by a two-tier mechanism involving the stabilization of pro-neural mRNAs by direct 3’UTR interaction and the repression of anti-neural mRNAs in a complex with neuronal miRISC. Together, our findings provide a rationale for future studies investigating the function of SYNCRIP in mammalian brain development and disease.

2021-05-05 | GSE149561 | GEO

RNA binding protein SYNCRIP regulates the leukemia stem cell program [RNA-Seq]

Project description:RNA binding proteins (RBPs) tightly control mRNA abundance, stability and translation while mutations or altered expression of specific factors can drive malignancy1,2. However, the identity of the RBPs that govern cancer stem cell self-renewal remains poorly characterized. The MSI2 RBP is a central regulator of translation of the cancer stem cell program3-5,6. Here we report, through proteomics analysis of the MSI2 interacting RBP network and functional shRNA screening, 24 genes required for in vivo leukemia, 20 of which are direct MSI2 protein interactors. Seven of these shRNA screen hits were retested in vitro and found to be required for myeloid colony formation. SYNCRIP (also known as HNRP-Q or NSAP1) was the most differentially required gene between normal (c-kit enriched cells) and myeloid leukemia cells. SYNCRIP is highly expressed in mouse and human leukemia cells and its depletion increases apoptosis, differentiation and delays leukemogenesis. Gene expression profiling of SYNCRIP depleted cells demonstrates a loss of the MLL-AF9 and HOXA9 leukemia stem cell gene associated program. SYNCRIP interacts with MSI2 indirectly through shared mRNA targets (such as Hoxa9, Myc and Ikzf2) and MSI2 or HOXA9 overexpression rescues the effects of SYNCRIP depletion. Strikingly, the shRNA-SYNCRIP gene expression signature can predict survival in AML patients. Overall, we uncovered a functionally dysregulated riboproteome in cancer that can be further distinguished from normal cells and propose that targeting this network could result in a novel therapeutic strategy in eradicating cancer stem cells.

2017-04-24 | GSE74178 | GEO

Protein expression profile of miR-33b overexpressing ES-2 cells upon OCM treatment

Project description:Omentum conditioned medium (OCM) is known to enhance ovarian cancer oncogenesis. In this study, miR-33b exerts tumor suppressive effects on ovarian cancer cells in response to omentum conditioned medium (OCM) treatment. To identify the molecular mechanism and main biological pathways involved in the tumor inhibiting activity by miR-33b in the ovarian cancer metastasis. To achieve this, miR-33b was stably overexpressed in ovarian cancer cell line ES-2, and the protein expression profile of miR-33b overexpressing ES-2 cells upon OCM treatment was determined.

2022-02-17 | PXD026901 | Pride

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