RNA-seq analysis of RNA-binding protein HuR knockout mice oral epithelial tissues
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ABSTRACT:
PROVIDER: PRJNA481058 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7521710.fastq.gz | Fastqsanger.gz | |||
| SRR7521705.fastq.gz | Fastqsanger.gz | |||
| SRR7521706.fastq.gz | Fastqsanger.gz | |||
| SRR7521707.fastq.gz | Fastqsanger.gz | |||
| SRR7521708.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: The goals of this study is to compare NGS-derived oral epithelial transcriptome profiling (RNA-seq) of WT and HuR KO tongue tissues exposed with carcinogen 4-nitroquinoline 1-oxide (4-NQO) induced oral tumorigenesis. Methods: Oral tongue tissues mRNA profiles of six-weeks old wild-type (WT) and epithelial HuR knockout (HuR−/−) mice exposed with 4NQO were generated by deep sequencing, in triplicate, using Illumina hiseq2500. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks - fill in William Results: There were no over-represented sequences, derived from primers and adapters from the library, and no bad quality nucleotides, the pre-process step was not necessary. On average, there were 64,096,543 reads per sample of 50 pair bases each. The alignment to the genome average rate of total mapped reads was 98.28%, which is a really good result considering we are working with Mouse data. There is a clear separation of the sample by the groups in the PCA plot and the samples cluster according by the groups in the identity plot. Nonetheless, Group B seems to be more heterogeneous, with sample Group_B-4_S4 showing signs of a hybrid expression profile that encompasses groups A and B. The system level analysis was made using iPathway Guide from Advaitabio. For system level analysis we used adjusted p value threshold of 0.1. A total of 32 pathways were considered statistically significant in an adjp threshold of 0.05. Interesting to note the presence of terms related to an altered function of the mitochondria. “ECM-receptor interaction” is changed with adj.p of 1.6 x 10-4. GO Biological term “epidermal cell differentiation” ” is changed with adj.p of 7.4 1.6 x 10-8. The gene Elavl1, although what seems to be a great expression in both group (baseMean = 2431.1 counts) have a log2 fold change of -0.2 and an adjp = 0.2. Number of DE genes Group-B_vs_Group-A adjp ≤ 0.1 = 5,849 DE genes adjp ≤ 0.01 = 2,258 DE genes Conclusions: Our study represents the first detailed analysis of HuR WT and HuR-/- oral epithelial tissue transcriptomes, with biologic replicates, generated by RNA-seq technology. Our results show that HuR controls subset of genes responsible for epithelial differentiation and energy metabolism. We conclude that HuR is critical factor in epithelial homeostasis.
2020-01-06 | GSE117095 | GEO
Project description:Here, we show that HuR cleavage is dependent on active caspase-3 in oral cancer cells treated with ionizing radiation and the chemotherapeutic drug paclitaxel. We determined that oral cancer cells overexpressing cyclooxygenase-2 (COX-2) limited the cleavage of both caspase-3 and HuR, which in turn, reduced the rate of apoptosis in paclitaxel treated cells. Specific inhibition of COX-2 by celecoxib promoted apoptosis through activation of caspase-3 and cleavage of HuR in paclitaxel-resistant oral cancer cells. In addition, oral cancer cells overexpressing cellular HuR increased the half-life of COX-2 mRNA and promoted COX-2 expression, exhibiting enhanced tumor growth in vivo in comparison with the cleavable form of HuR. Finally, our RNP IP and RNA transcriptome analysis of HuR under IR revealed that the HuR cleavage product-1 (HuR-CP1) associates and promotes the expression of mRNAs encoding proteins involved in apoptosis.
2017-02-14 | GSE79477 | GEO
Project description:ionPurpose: The goal of this study is to investigate how HuR regulates NASH progression. Methods: The hepatic mRNA profiles of HuR flox/flox and hepatocyte-specific HuR knockout (HKO) mice (n=3 for each group) fed with an MCD for 3 weeks were generated by deep sequencing using an Illumina Novaseq platform. Paired-end clean reads were aligned to the mouse reference genome(Ensemble_GRCm38.p6) with TopHat (version 2.0.12), and the aligned reads were used to quantify mRNA expression by using HTSeq-count (version 0.6.1). Conclusion: Our study represents the first detailed analysis of hepatic mRNA profiles in HuR flox/flox and hepatocyte-specific HuR knockout (HKO) mice fed with an MCD for 3 weeks, generated by RNA-seq technology. Our results show that 353 genes were upregulated and 422 genes were downregulated. Gene Ontology (GO) analysis showed that genes related to leukocyte migration, leukocyte chemotaxis, cell chemotaxis, neutrophil migration and Fc receptor signaling pathway were significantly decreased, which contributes to the protective effects of NASH progression in HKO mice.
2023-06-17 | GSE152670 | GEO
Project description:NAFLD has become the most common chronic liver disease worldwide. Human antigen R (HuR), an RNA-binding protein, is an important post-transcriptional regulator. HuR has been reported as a key player in regulating lipid homeostasis in the liver and adipose tissues by using tissue-specific HuR knockout mice. However, the underlying mechanism by which hepatocyte-specific HuR regulates hepatic lipid metabolism under metabolic stress remains unclear and is the focus of this study.
2022-12-01 | GSE213215 | GEO
Project description:Human antigen R (HuR) is a member of the Hu family of RNA-binding proteins and is involved in many physiological processes. To investigate the role of adipose HuR, we generate adipose-specific HuR knockout (HuRAKO) mice. As compared with control mice, HuRAKO mice show obesity when induced with a high-fat diet, along with insulin resistance, glucose intolerance, hypercholesterolemia and increased inflammation in adipose tissue. The obesity of HuRAKO mice is attributed to adipocyte hypertrophy in white adipose tissue due to decreased expression of adipose triglyceride lipase (ATGL), a critical lipase involved in lipolysis. HuR positively regulates ATGL expression by promoting the mRNA stability and translation of ATGL. Consistently, the expression of HuR in adipose tissue is reduced in obese humans, which is associated with reduced ATGL expression. This study suggests that adipose HuR may be a critical regulator of ATGL expression and lipolysis and thereby controls obesity and metabolic syndrome.
2019-04-23 | GSE130147 | GEO
Project description:BackgroundHuR/ELAV1, a ubiquitous RNA-binding protein, belongs to the RNA-binding protein family and is crucial for stabilizing and regulating the translation of various mRNA targets, influencing gene expression. Elevated HuR levels are associated with multiple disorders, including cancer and neurodegenerative diseases. Despite the identification of small molecule inhibitors targeting HuR, their detailed characterization remains limited. Recently, Eltrombopag, an FDA-approved drug for immune thrombocytopenic purpura and chemotherapy-induced thrombocytopenia, emerged as a potential HuR inhibitor. However, the specific molecular pathways influenced by both HuR and Eltrombopag are not fully understood. ResultsOur study demonstrates that Eltrombopag operates via HuR inhibition, affecting gene expression regulation at the posttranscriptional level. We show that both HuR knockout and Eltrombopag treatment modulate iron metabolism by decreasing ferritin heavy chain (FTH1) and light chain (FTL) synthesis while increasing the expression of Iron-regulatory protein 2 (IRP2), a key regulator of ferritin translation. Additionally, HuR inhibition reduces the levels of Glycoprotein Hormones, Alpha Polypeptide (CGA), a marker associated with hormone-induced tumors, suggesting a potential use of Eltrombopag in treatment of cancers overexpressing CGA. We observed that the main of control is manifested at the level of translation inhibition, with proteosome-mediated regulation also playing an important role.ConclusionsThese findings uncover novel posttranscriptional mechanisms governed by HuR and its inhibitor, elucidating pathways relevant to HuR-mediated regulation and molecular therapies aimed at targeting this protein.
2024-12-20 | PXD050698 | Pride
Project description:Human antigen R (HuR) protein, a RNA binding protein (RBP), has been reported to regulate essential steps in RNA metabolism and immune response in a variety of cell types, but its function in metabolism remains unclear. This study identifies HuR as a major repressor during adipogenesis. Knockdown and overexpression of HuR in primary adipocyte culture enhances and inhibits adipogenesis in vitro, respectively. Fat-specific knockout of HuR significantly enhances adipogenic gene program in all three major adipose tissues including epidydimal, inguinal white and brown adipose tissue, accompanied with systemic glucose intolerance and insulin resistance. Conversely, transgenic overexpression of HuR in adipose tissue prevents the HFD induced obesity by repressing adipogenesis. Mechanistically, HuR may inhibit adipogenesis by recognizing and modulating the stability of hundreds of adipocyte transcripts, including the mRNA of Insig1, a negative regulator during adipogenesis. Taken together, our work establishes HuR as a novel posttranscriptional regulator of adipogenesis and provides a new insight into how RNA processing contributes to adipocyte development.
2019-09-09 | GSE124278 | GEO
Project description:Human antigen R (HuR) protein, a RNA binding protein (RBP), has been reported to regulate essential steps in RNA metabolism and immune response in a variety of cell types, but its function in metabolism remains unclear. This study identifies HuR as a major repressor during adipogenesis. Knockdown and overexpression of HuR in primary adipocyte culture enhances and inhibits adipogenesis in vitro, respectively. Fat-specific knockout of HuR significantly enhances adipogenic gene program in all three major adipose tissues including epidydimal, inguinal white and brown adipose tissue, accompanied with systemic glucose intolerance and insulin resistance. Conversely, transgenic overexpression of HuR in adipose tissue prevents the HFD induced obesity by repressing adipogenesis. Mechanistically, HuR may inhibit adipogenesis by recognizing and modulating the stability of hundreds of adipocyte transcripts, including the mRNA of Insig1, a negative regulator during adipogenesis. Taken together, our work establishes HuR as a novel posttranscriptional regulator of adipogenesis and provides a new insight into how RNA processing contributes to adipocyte development.
2019-09-09 | GSE124275 | GEO
Project description:Human antigen R (HuR) protein, a RNA binding protein (RBP), has been reported to regulate essential steps in RNA metabolism and immune response in a variety of cell types, but its function in metabolism remains unclear. This study identifies HuR as a major repressor during adipogenesis. Knockdown and overexpression of HuR in primary adipocyte culture enhances and inhibits adipogenesis in vitro, respectively. Fat-specific knockout of HuR significantly enhances adipogenic gene program in all three major adipose tissues including epidydimal, inguinal white and brown adipose tissue, accompanied with systemic glucose intolerance and insulin resistance. Conversely, transgenic overexpression of HuR in adipose tissue prevents the HFD induced obesity by repressing adipogenesis. Mechanistically, HuR may inhibit adipogenesis by recognizing and modulating the stability of hundreds of adipocyte transcripts, including the mRNA of Insig1, a negative regulator during adipogenesis. Taken together, our work establishes HuR as a novel posttranscriptional regulator of adipogenesis and provides a new insight into how RNA processing contributes to adipocyte development.
2019-09-09 | GSE124279 | GEO
Project description:We report the HuR-RNA interactions in the liver by performing RNA-immunoprecipitation sequencing (RIP-seq). RIP-seq was performed in healthy livers of wildtype (WT) mice using a HuR antibody. We found that 1380 cytoplasmic-target mRNAs bound to HuR, as assessed by the comparison between the HuR-specific antibody and the IgG control
2021-09-15 | GSE143703 | GEO