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Genome wide analysis of mRNA expression and polysome profiling in DDX3 knockdown SAS cells

ABSTRACT: By analyzing the RNAseq and RIBOseq results, we identified potential pathways for DDX3 to remodel tumor microenviroment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE160803 | GEO | 2020/11/05

REPOSITORIES: GEO

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SAS cells: control siRNA (siC) vs DDX3 siRNA (siD) transfected

Project description:Transcriptional profiling of SAS cells comparing siC-transfected SAS cells with siD-transfected SAS cells. The latter decreased proliferation and migration of SAS cells. Goal was to determine the DDX3-regulated transcripts.

2018-04-17 | GSE113183 | GEO

Genome wide analysis of mRNA expression and polysome profiling in DDX3 knockdown SAS cells

Project description:Genome wide analysis of mRNA expression and polysome profiling in DDX3 knockdown SAS cells

| PRJNA674567 | ENA

Profiles of ribosome-associated mRNAs regulated by expression of wild-type (WT) or R534H variant of DDX3 with or without Sodium Arsenite treatment [Ribo-Seq]

Project description:By using ribosome profiling, we demonstrate that catalytic activity of the RNA helicase DDX3 is generally required for mediating translation repression under stress. Intriguingly, however, a cancer-related DDX3 variant DDX3 R534H selectively preserves translation of genes encoding core nucleosome components. Additionally, DDX3 variants also shift ORF usage on select genes, such as RPLP1 and stress-response factors as an added mechanism of translation regulation during stress. Thus, DDX3 through both extensive and selective interactions with RNA and the ribosomal machinery helps to remodel the translational landscape under stress and in cancer.

2016-04-21 | GSE70802 | GEO

mRNA-seq data for DDX3 knockdown in murine hepatocytes in vivo and in vitro

Project description:A transcriptome analysis was performed to estimate a primary response of the hepatocytes to depletion of DDX3 RNA helicase both in vitro and in vivo. We used two siRNAs with different efficacy and demonstrated protein level-dependent effects on DDX3 RNA helicase depletion in the murine liver. We found that strong reduction of DDX3 protein (>85%) leads to similar changes in vitro and in vivo – we observed deregulation of cell cycle, Wnt and cadherin pathways. However, more modest downregulation of DDX3 protein (60-65%) resulted in discordant results between gene expression in vitro and in vivo – in vitro data were close to those under strong reduction, while in vivo phenotype was weak. These results demonstrate that the level of active DDX3 protein can dramatically influence on the phenotype in vivo, which should be taken into account during drug development.

2021-06-29 | GSE178618 | GEO

Microarray expression profile from YAP1 knockdown in DDX3-overexpressing colorectal cancer cells

Project description:To identify which genes could be modulated by the DDX3-YAP1 axis in SW48 cells.

2016-10-18 | GSE88851 | GEO

SAS cells: control siRNA (siC) vs DDX3 siRNA (siD) transfected

Project description:SAS cells: control siRNA (siC) vs DDX3 siRNA (siD) transfected

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A new role for the DEAD-box RNA helicase DDX3 in co-translational protein quality control

Project description:DEAD-box RNA helicases are central players in RNA metabolism, however, their role in translation regulation is largely unexplored in parasitic protozoa. Here, we have investigated the role of DDX3 RNA helicase in ribosome-associated protein quality control in Leishmania. We show that ribosomes move more slowly and de novo polypeptide synthesis is reduced in cells lacking DDX3. In accordance with the slowing of ribosome speed, DDX3 depleted cells exhibit higher levels of ribosome-associated ubiquitination. Especially, ubiquitination of nascent polypeptides is enhanced upon DDX3 loss as determined by the isolation of ribosome-associated nascent chains modified either by HA-Ubiquitin or by endogenous ubiquitin using biotinylated-puromycin labeling. Consistent with increased co-translational ubiquitination, quantitative proteomics analysis revealed higher recruitment of E3 ubiquitin ligases and proteasomal components to DDX3 knockout ribosomes to eliminate aberrant nascent polypeptides. In addition, we show that cells lacking DDX3 accumulate cytosolic aggregates. This along with the higher recruitment of ribosome-associated chaperones and the improvement of translation by increasing HSP70 availability suggests that co-translational control of nascent polypeptides is impaired in the absence of DDX3. Altogether, these results highlight an important role for DDX3 in ribosome-associated quality control by reducing co-translational ubiquitination and proteotoxicity, hence allowing optimal ribosome movement and translation elongation.

2021-07-23 | PXD020667 | Pride

Dual targeting of DDX3 and eIF4A by the translation inhibitor rocaglamide A

Project description:Small molecule compounds that sense the nucleic acid sequences, promise the attractive venue for drug development. Such an unusual effect has been observed in the natural product Rocaglamide A (RocA) from Aglaia plant, proving to exhibit anti-tumor effects by clamping eukaryotic initiation factor (eIF) 4A onto mRNA polypurine sequences. Although eIF4A has been speculated the unique target of RocA, the insensitization of eIF4A in human cells only partially rescued the translation repression from RocA, suggesting another alternative target of this compound. Here, we revealed that DDX3 is an alternative target of RocA. Developing a RocA derivative with an O-nitrobenzoxadiazole unit (RocA-O-NBD), which can covalently bind to proximate proteins and provide fluorescence to them, we identified DDX3 bound to RocA. As observed in eIF4A, RocA locked the DDX3 protein onto polypurine sequences of RNA in an ATP-independent manner. De novo assembled Aglaia plant transcriptome uncovered the natural amino acid substitutions in Aglaia DDX3 to protect itself from RocA toxicity. Because of the dominant negative effect of RocA, we also proved the protein abundance of eIF4A and DDX3 in cancer cells determines their sensitivity to RocA. Overall, this study discovered DDX3 as another target of RocA and suggests the probability to predict tumor toxicity of RocA by the target abundance.

2020-12-07 | GSE148636 | GEO

DDX3 depletion represses translation of mRNAs with complex 5′ UTRs

Project description:We describe the subset of transcripts that require DDX3 for efficient translation.

2019-03-25 | GSE125114 | GEO

Effect of DDX3 inhibitors on CD4+ T cells

Project description:An innovative approach to eliminate HIV-1-infected cells emerging out of latency, the major hurdle to HIV-1 cure, is to pharmacologically reactivate viral expression and concomitantly trigger intracellular pro-apoptotic pathways in order to selectively induce cell death (ICD) of infected cells, without reliance on the extracellular immune system. In this work we demonstrate the effect of DEAD-box polypeptide 3, X-Linked (DDX3) inhibitors on selectively inducing cell death in latent HIV-1-infected cell lines, primary CD4+ T cells and in CD4+ T cells from cART-suppressed people living with HIV-1 (PLWHIV). RNA sequencing analysis revealed that while overall gene expression was minimally dysregulated, DDX3 inhibition in independent donor CD4+ T cells led to significant downregulation of BIRC5 and HSPB1A, genes critical to cell survival during HIV-1 infection. We used single-cell FISH-Flow technology to characterise latency reversal and the contribution of viral RNA to inducing cell death; pharmacological targeting of DDX3 induced HIV-1 RNA expression, resulting in phosphorylation of IRF3, upregulation of IFNβ and selective induction of apoptosis in viral RNA-expressing CD4+ T cells from PLWHIV but not bystander cells. DDX3 inhibitor treatment of CD4+ T cells from PLWHIV in an in vitro culture model over five days resulted in an approximately 50% reduction of the inducible latent HIV-1 reservoir as determined by quantitation of CA HIV-1 RNA, by TILDA, as well as by FISH-Flow technology. Our data support the translation of DDX3 inhibitor class compounds into HIV-1 curative strategies and provide proof of concept for pharmacological reversal of latency coupled to induction of apoptosis towards elimination of the inducible reservoir.

2021-02-26 | GSE167553 | GEO

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