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HuR-dependent translation efficiency (TE) and mRNA expression analysis in hypoxia.

ABSTRACT: mRNA TE and steady-state levels were measured in hypoxic U87MG cells treated with non-silencing control or HuR-specific siRNA pools followed by ribosome density fractionation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE128541 | GEO | 2020/04/23

REPOSITORIES: GEO

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HIF-2α- and HIF-1α-dependent translation efficiency (TE) and mRNA expression analysis in hypoxia.

Project description:mRNA TE and steady-state levels were measured in hypoxic U87MG cells treated with non-silencing control or HIF-2α-specific or HIF-1α-specific siRNA pools followed by ribosome density fractionation.

2020-04-23 | GSE128555 | GEO

Hypoxia-Acidosis translation efficiency (TE) and mRNA expression analysis

Project description:mRNA TE and steady-state levels were measured in normoxic, normoxia-acidosis, hypoxia, hypoxia acidosis U87MG from RNA seq of ribosome density fractionation.

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Oxygen-dependent translation efficiency (TE) and mRNA expression analysis

Project description:mRNA TE and steady-state levels were measured in U87MG cells subjected to 21% or 1% oxygen followed by ribosome density fractionation.

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HuR-dependent translation efficiency (TE) and mRNA expression analysis in hypoxia.

Project description:HuR-dependent translation efficiency (TE) and mRNA expression analysis in hypoxia.

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Cytoplasmic overexpression of RNA-binding protein HuR in meningioma is a marker of poor prognosis and specific HuR knockdown decreases meningioma cell growth and resistance to hypoxia

Project description:HuR is known to regulate mRNA stability and translatability in cytoplasm. In several human tumors, the level of HuR expression has been shown to correlate with poor disease outcome. In meningioma, however, the prognostic value and the potential pro-oncogenic properties of HuR remain obscure. To clarify these, transcriptome-wide analyses in IOMM-Lee cells were performed to pinpoint the detailed molecular consequences of HuR knockdown. In IOMM-Lee cells, transcriptomic analyses revealed that HuR knockdown deregulated the signaling pathway of HIF1A and upregulated the expression of genes for cytoplasmic mRNA processing body assembly, poly(A)-specific ribonuclease activity, positive regulation of apoptosis, negative regulation of RNA splicing, global genome nucleotide-excision repair, and positive regulation of cell cycle arrest. Interestingly, HuR knockdown under hypoxic culture condition potentiated further the effects of HuR knockdown on cell growth, apoptosis, and HIF1A expression.

2017-05-11 | GSE95212 | GEO

Hypoxia-Acidosis translation efficiency (TE) and mRNA expression analysis

Project description:Hypoxia-Acidosis translation efficiency (TE) and mRNA expression analysis

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Hypoxia-induced circPLOD2a/b promote migration and invasion of GBM cells via suppressing XIRP1 through binding to HuR [1]

Project description:Background. Glioblastoma (GBM) is the most lethal form of brain tumors in human adults, and hypoxia is a common microenvironment in this disease. Circular RNAs (circRNAs) are identified as regulators in cancers including GBM. However, the specific roles of circRNAs in GBM under hypoxic condition remains elusive. Methods. RNA-seq was employed to investigate the expression profile of circRNAs in U87 cells under normoxia and hypoxia. Two circRNAs spliced from the same parental gene, named as circPLOD2a and circPLOD2b, were identified as hypoxia-responsive circRNAs, whose circular structures were verified by, qRT-PCR, RNase R digesting and Sanger sequencing in U87. Knockdown and overexpression of circPLOD2a/b in GBM cells were used to investigate the biological functions of these two circRNAs on tumor progression. Fluorescence in situ hybridization, RNA-pull down, mass spectrometry and RNA immunoprecipitation assays were conducted to explore the interactions between circPLOD2a/b, human antigen R (HuR), xin actin binding repeat containing 1 (XIRP1). Results. CircPLOD2a/b were significantly up-regulated in hypoxic GBM cells and directly induced by HIF1α under hypoxia. Overexpression of circPLOD2a/b enhance GBM cell invasion and migration, which could be inhibited by circPOD2a/b knockdown. Mechanistically, circPLOD2a/b competitively bind to HuR, inhibiting the interaction between HuR and XIRP1, thus promoting the tumor aggressiveness in GBM both in vitro and in vivo through down-regulating XIRP1. Conclusions. Hypoxia-induced circPLOD2a/b were identified as key regulators of migration and invasion in GBM cells, and act as oncogenic circRNAs to attenuate the interaction between HuR and XIRP1, which may be potential therapeutic strategy for GBM treatment.

2023-10-23 | GSE245634 | GEO

Hypoxia-induced circPLOD2a/b promote migration and invasion of GBM cells via suppressing XIRP1 through binding to HuR [2]

2023-10-23 | GSE245635 | GEO

A genome-wide CRISPR screen identifies HuR as a regulator of apoptosis induced by dsRNA and viral infection

Project description:Cell death is an important host defense in response to viral infections. In this study,we performed an unbiased whole-genome CRISPR/Cas9 screen in A549 lung adenocarcinoma cells to identify potential regulators involved in cell death triggered dsRNA, a common byproduct of viral replication. Of several top candidate genes, we identified the RNA binding protein ELAV like protein 1 (ELAVL1) (ELAVL1, also called HuR) that encodes Hu antigen R (HuR). Depletion of HuR by gene editing led to less cell death induced by dsRNA. We further demonstrated that HuR regulated apoptosis, and the RNA recognition motif (RRM) 3 of HuR was essential for its proapoptotic function. HuR bound mRNA of anti-apoptotic gene BCL2. HuR depletion had no influence on BCL2 mRNA levels, but instead downregulated the BCL2 translation. Polysome fractionation studies showed that HuR retarded the BCL2 mRNA in the non-translating pool of polysomes. Moreover, protection from dsRNA-induced apoptosis by HuR depletion required the presence of BCL2, indicating that the proapoptotic function of HuR is executed by suppressing BCL2. Consistently, HuR regulated apoptosis induced by infection of encephalomyocarditis or Semliki Forest virus, two unrelated positive strand RNA viruses. Collectively, our work identified a suite of proteins that regulate dsRNA-induced cell death, and elucidated the mechanism by which HuR acts as a pro-apoptotic factor.

2021-01-28 | GSE165625 | GEO

HuR (ELAVL1) RIP-chip and knockdown exon array

Project description:Integrative regulatory mapping indicates that the RNA-binding protein HuR (ELAVL1) couples pre-mRNA processing and mRNA stability In this dataset, we employed two distinct experiments. 1) HuR RIP-chip to identify mRNA targets of HuR. 2) HuR knockdown to identify mRNAs whose expression are dependent on HuR. All 12 samples were normalized with PLIER using Affymetrix power tools. To identify RNA targets of HuR, HuR RIP samples were compared to Mock RIP samples. To identify RNA regulated by HuR, HuR knockdown samples were compared to mock knockdown samples.

2011-08-18 | E-GEOD-29778 | biostudies-arrayexpress

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