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Expression data from human A549 cells with or without circRNA-FOXO3 overexpression

ABSTRACT: Expression data from human A549 cells with or without circRNA-FOXO3 overexpression

PROVIDER: PRJNA756950 | ENA |

REPOSITORIES: ENA

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Expression data from human A549 cells with or without circRNA-FOXO3 overexpression

Project description:To reveal the changes of miRNAs in A549 cells transfected with circRNA-FOXO3, we have employed miRNA microarray expression profiling.

2021-08-24 | GSE182576 | GEO

Constitutively Active Foxo3 in Oocytes Preserves Ovarian Reserve in Mice

Project description:During female reproductive life, the reserve of ovarian follicles is reduced by maturation and atresia until menopause ensues. Foxo3 is required to maintain the ovarian reserve in mice. We asked if overexpression of a constitutively active FOXO3 protein can increase long-lasting ovarian reproductive capacity in mice. Trangenic vs non-transgenic mice onto Foxo3+/- vs Foxo3-/- genotype

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FOXO3 regulates Smad3 and Smad7 through SPON1 circular RNA to inhibit idiopathic pulmonary fibrosis

Project description:Forkhead box protein O3 (FOXO3) has good inhibition ability toward fibroblast activation and extracellular matrix, especially for the treatment of idiopathic pulmonary fibrosis. How FOXO3 regulates pulmonary fibrosis remains unclear. In this study, we reported that FOXO3 had binding sequences with F-spondin 1 (SPON1) promoter, which can activate its transcription and selectively promote the expression of SPON1 circRNA (circSPON1) but not mRNA expression. We further demonstrated that circSPON1 was involved in the extracellular matrix deposition of HFL1. In the cytoplasm, circSPON1 directly interacted with TGF-β-induced Smad3 and inhibited the activation of fibroblasts by inhibiting nuclear translocation. Moreover, circSPON1 bound to miR-942-5p and miR-520f-3p that interfered with Smad7 mRNA and promoted Smad7 expression. This study revealed the mechanism of FOXO3 in the occurrence and development of pulmonary fibrosis. Potential therapeutic targets and new insights into the diagnosis and treatment of idiopathic pulmonary fibrosis based on circRNA were also provided.

2021-09-10 | GSE183750 | GEO

Detection of circRNA in Drosophila Fly heads and S2 cells using RNA-seq with or without RNaseR tretment

Project description:We determined circRNA abundance in fly Heads and S2 cells by generating and analyzing high-throughput RNA-sequencing libraries prepared from rRNA-depleted RNA. In order to determine whether the observed sequencing reads are due to bona fide circRNAs, we pre-treated the RNA with RNAse-R before the rRNA-depletion procedure. Indeed, most of the identified circRNAs were more enriched in comparison to the canonical mRNA isoforms following the RNAse-R treatment. We compare circRNA levels in wt (Canton S) flies with flies carrying the C4 ("slow polymerase") mutation. 4 samples of Drosophila Canton S and 4 samples of flies carrying the C4 ("slow polymerase") mutation. For each sample, one library was prepared from RNA after RNaseR treatment and the second from RNA with without treatment (mock). RNA library from one Canton Sample was used for stranded libray preprepation.

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human circRNA binding proteins in neuroblastoma

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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Transcriptional responses to SAMD9 overexpression in A549 cells

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2024-12-31 | GSE228684 | GEO

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