Analysis of circRNA expression profiles in U937 cells after p62 knockdown
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ABSTRACT:
PROVIDER: PRJNA909176 | ENA |
REPOSITORIES: ENA
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Project description:The aim of this study was to investigate the effect of p62 on circRNA and mRNA expression profiles in U-937 cells.
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Project description:circRNA profiles of diabetic retinopathy
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Project description:ZXDC1 augments the expression of various markers of monocyte/macrophage differentiation when over-expressed in the U937 cell line treated with the phorbol ester PMA. Likewise, knockdown of ZXDC1 restricts the induced expression of these markers. We sought to identify specfic gene targets of ZXDC1 during the process of monocyte/macrophage differentiation in U937 by performing gene expression profiling in cells exhibiting reduced expression of ZXDC1 compared to controls. We used microarray to identify genes regulated by ZXDC during PMA-induced differentiation of U937 monoblasts towards a monocyte/macrophage phenotype An inducible shRNAmir (Tet-On) cell line was established in the U937 background that displayed significant, reproducible, and doxycycline inducible knockdown of ZXDC1. Using this cell line, we created four experimental groups to identify gene targets of ZXDC1 during PMA-induced differention towards a monocyte/macrophage phenotype: Vehicle alone; Vehicle+Doxycycline; PMA alone; PMA+Doxycycline. Each independent group was used for RNA extraction and hybridization on Affymetrix microarray chips.
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Project description:Previously, we identified ARIH2, the gene encoding Triad1, as a HoxA10 target gene. We found that HoxA10-induced expression of Triad1 was necessary for termination of emergency granulopoiesis, and antagonized leukemogenesis in a murine model of KMT2A-rearranged AML. In this study, we found that knockdown Triad1 increased polysome-specific mRNAs regulating the cellular response to stress, the DNA-damage response, ribosomal biogenesis, or protein catabolism, but decreased mRNAs regulating mitosis, DNA-repair, DNA and RNA metabolism, or Tp53 activity in U937 cells. Polysome-specific mRNAs for Solute Carrier Proteins (SLCs) were also increased by Triad1-knockdown, consistent with correction of metabolic defects during the ISR. This included SLCs involved in import of amino acids, long chain fatty acids and glucose, and lactate export. In comparison of polysome-specific mRNA profiles with Triad1-knockdown versus knockdown of Triad1 plus Gcn1, we identified the same gene and pathway differences as in comparison of Triad1-knockdown to control cells. There were only minor differences in polysome specific mRNAs in cells with Triad1- plus Gcn1-knockdown versus control cells, encompassing fewer differences than with Triad1-knockdown alone. This suggested that Triad1-knockdown on ribosome/polysome profiles are reversed by Gcn1-knockdown in U937 cells.
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Project description:Gene expression profiling of U937 cells upon knockdown of the DEK oncogene by two different shRNAs (shDEK14 and shDEK17). The DEK oncogene was knocked down by shRNA to study the changes in gene expression.
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Project description:To compare the circRNA expression profile of diabetic retinopathy with that of diabetes mellitus and controls, peripheral blood mononuclear cell samples were obtained and extracted from healthy controls and diabetes mellitus patients (with or without diabetic retinopathy). CircRNA Capital Bio Technology Human CircRNA Array v2 was performed to detect circRNA expression profiles. To further check differentiate circRNA, qRT_PCR assay was performed to detect the level of 5 candidates.
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Project description:Circular RNAs (circRNAs), a noncoding RNA class originating from alternative splicing, are highly abundant in neural tissues and were shown to regulate gene expression e.g. by interacting with microRNAs and RNA-binding proteins. Neuroblastoma is an embryonal neoplasia, which arises from undifferentiated neural crest cells. Here, we aimed to explore, whether circRNAs influence the pathogenesis of high-risk neuroblastoma. We performed whole-transcriptome sequencing of 104 primary neuroblastoma samples of all risk-groups and identified 5,203 unique circRNAs involving 2,302 genes. Candidate circRNA expression did not correlate with host gene expression, indicating independent regulatory mechanisms. circRNAs were significantly downregulated in the MYCN-amplified high-risk tumors. These findings were independently reproduced in a tetracycline-inducible MYCN-overexpression system based on a non MYCN-amplified neuroblastoma cell line, suggesting that MYCN drives this global circRNA repression. We identified the RNA helicase DHX9 as a mediator of this global suppressive effect of MYCN on circRNAs. Comparing our RNA sequencing data with other cancers and controls revealed a circRNA subset specifically upregulated in neuroblastoma that included a circRNA derived from the ARID1A tumor suppressor gene. Specific circARID1A knockdown resulted in reduced proliferation, cell numbers and viability, prompted apoptosis and induced a differentiated phenotype. Neither knockdown, nor overexpression of circARID1A influenced ARID1A mRNA and protein levels significantly. To dissect the potential mode of function, we performed a pulldown assay with subsequent mass spectrometry. We identified the RNA-binding protein KHSRP as an interaction partner that participates in the mechanism of action of circARID1A. In summary, this study highlights an important role of circRNAs in neuroblastoma biology and may establish this RNA class as a future therapeutic target and biomarker.
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