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CircHIPK3 and FMRP compete for direct binding to BRCA1 mRNA controlling its protein levels and DNA damage response

ABSTRACT: CircHIPK3 and FMRP compete for direct binding to BRCA1 mRNA controlling its protein levels and DNA damage response

PROVIDER: PRJNA1032074 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26521333_1.fastq.gz	Fastqsanger.gz
	SRR26521333_2.fastq.gz	Fastqsanger.gz
	SRR26521334_1.fastq.gz	Fastqsanger.gz
	SRR26521334_2.fastq.gz	Fastqsanger.gz
	SRR26521335_1.fastq.gz	Fastqsanger.gz

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CircHIPK3 and FMRP compete for direct binding to BRCA1 mRNA controlling its protein levels and DNA damage response [miRNA_pulldown]

Project description:Circular RNAs (circRNAs) are covalently closed RNA molecules widely expressed in eukaryotes and regulated in several pathological processes, including cancer. Many studies point to their mechanism of action as miRNA and protein sponges; however, we propose a new functionality based on circRNA-mRNA interaction to regulate mRNA fate. We show that the widely expressed circHIPK3 directly interacts in vivo with the BRCA1 mRNA through the back-splicing region. This interaction favoured the translation of BRCA1 by competing for the binding of the FMRP1 RNA-binding protein, which acts as a repressor of BRCA1 translation. CircHIPK3 depletion or disruption of the CircRNA-mRNA interaction decreased BRCA1 levels and increased DNA damage, sensitizing several cancer cell lines to DNA-damage-inducing agents and rendering them susceptible to synthetic lethality. Additionally, mimicking circHIPK3 interaction with lock-nucleic acid (LNA) oligonucleotides restores BRCA1 levels in hereditary breast cancer model cells, underscoring circRNA-mRNA interaction’s importance in regulating cell homeostasis and drug response.

2024-09-13 | GSE246225 | GEO

CircHIPK3 and FMRP compete for direct binding to BRCA1 mRNA controlling its protein levels and DNA damage response [RNA_pulldown]

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CircHIPK3 and FMRP compete for direct binding to BRCA1 mRNA controlling its protein levels and DNA damage response [RNA_pulldown]

Project description:CircHIPK3 and FMRP compete for direct binding to BRCA1 mRNA controlling its protein levels and DNA damage response [RNA_pulldown]

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CircHIPK3 and FMRP compete for direct binding to BRCA1 mRNA controlling its protein levels and DNA damage response [miRNA_pulldown]

Project description:CircHIPK3 and FMRP compete for direct binding to BRCA1 mRNA controlling its protein levels and DNA damage response [miRNA_pulldown]

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CircHIPK3 and FMRP compete for direct binding to BRCA1 mRNA controlling its protein levels and DNA damage response

Project description:This SuperSeries is composed of the SubSeries listed below.

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Effects of circHIPK3 silencing on mRNA expression

Project description:circHIPK3 silencing impairs ß-cell functions leading to a decrease in insulin secretion, proliferation, and survival. Therefore, we wanted to identify the mode of action of circHIPK3 by measuring gene expression changes upon circHIPK3 silencing in MIN6B1 cells.

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Project description:Aortic valve calcific disease (CAVD) is a common heart valve condition typically characterized by severe narrowing of the aortic valve. Our previous research has shown that circHIPK3 is downregulated in calcified aortic valve tissues and plays a role in regulating the progression of CAVD. To further investigate how circHIPK3 exerts its inhibitory effects on aortic valve calcification, we overexpressed circHIPK3 in aortic valve interstitial cells and conducted RNA-seq analysis, revealing that circHIPK3 regulates key factors in the Wnt signaling pathway. These findings contribute to a deeper understanding of the molecular mechanisms underlying CAVD, particularly the potential involvement of circRNAs in this disease.

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Role of FMRP in neurogenesis

Project description:Fragile X syndrome (FXS) is a rare disease but is the most common form of inherited intellectual disability and a leading cause of autism. FXS is due to the absence of the Fragile X Mental Retardation Protein (FMRP), an RNA-binding protein mainly involved in translational control. Even if this molecular defect is known, no specific therapy is available for FXS. The first alteration observed in the brain of FXS patients and of Fmr1 KO mice, model for FXS, is represented by an abnormal dendritic morphology that is associated with an altered synaptic plasticity. These findings led to numerous studies focused on mature neurons. However, recently, an increasing body of evidence is pointing out the importance of FMRP in the early steps of brain development. Thus, with the purpose to decipher the earliest molecular events leading to FXS we developed a stem-cell-based disease model by knocking-down the expression of Fmr1 in mouse embryonic stem (ES) cells. To gain insights in the pathways that are affected when FMRP is repressed, we performed a gene expression profile analysis comparing total RNA from shFmr1 and shControl ES cells using whole genome mouse microarrays. Transcripts were clustered according to their Gene Ontology classification using the DAVID software. Surprisingly, the most altered functional category was Nervous system development and function, highlighting the role of FMRP also during the earliest steps of neural development. To study the precise role of FMRP in Embryonic stem (ES) cells, we used an RNAi-based loss-of-function strategy by transducing mouse ES cells with a lentivirus expressing GFP and a shRNA targeting the constitutive exon 1 of Fmr1 (shFmr1). A random shRNA (shCT) was used as a control sequence. Transduced cells were sorted by flow cytometry and established as non-clonal cell populations. RNA samples were harvested and profiling experiments were performed in â??dye-balanceâ?? as indicated for each replicate.

2016-07-04 | E-GEOD-71184 | biostudies-arrayexpress

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