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The novel circle-RNA ZNF208 regulates the proliferation of cervical cancer fibroblasts through a ceRNA network

ABSTRACT: The novel circle-RNA ZNF208 regulates the proliferation of cervical cancer fibroblasts through a ceRNA network

PROVIDER: PRJNA849660 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19666450_1.fastq.gz	Fastqsanger.gz
	SRR19666450_2.fastq.gz	Fastqsanger.gz
	SRR19666451_1.fastq.gz	Fastqsanger.gz
	SRR19666451_2.fastq.gz	Fastqsanger.gz
	SRR19666452_1.fastq.gz	Fastqsanger.gz

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The novel circle-RNA ZNF208 regulates the proliferation of cervical cancer fibroblasts through a ceRNA network

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Project description:Long non-coding RNAs (lncRNAs) have been extensively studied as key regulators of cancer development in various cancers. *** is a newly identified lncRNA in recent years, and several studies have shown that *** may play oncogenic or anti-oncogenic roles in different cancers. Pan-cancer analysis showed that high *** expression was significantly associated with better prognosis. Nevertheless, the role of *** in the development of cervical cancer is unclear. In our study, we constructed a *** overexpression model in HeLa cell line. We found that *** overexpression significantly inhibited cell proliferation and induced apoptosis, and *** may be a novel anti-oncogenic factor in cervical cancer. Mechanistically, overexpression of *** could activate type I interferon signaling pathways and inhibits the expression of genes involved in DNA damage responses. Meanwhile, *** could regulate the expression of a large number of RNA binding protein genes thereby potentially affecting the alternative splicing of genes involved in cell proliferation or apoptosis regulation. We also established a ceRNA network to predict the regulatory effect of *** on gene expression through miRNA. Our study highlights the essential role of lncRNA *** in the development of cervical cancer and suggests the potential regulatory mechanisms.

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Project description:Long non-coding RNAs (lncRNAs) have been extensively studied as key regulators of cancer development in various cancers. TP53TG1 is a newly identified lncRNA in recent years, and several studies have shown that TP53TG1 may play oncogenic or anti-oncogenic roles in different cancers. Pan-cancer analysis showed that high TP53TG1 expression was significantly associated with better prognosis. Nevertheless, the role of TP53TG1 in the development of cervical cancer is unclear. In our study, we constructed a TP53TG1 overexpression model in HeLa cell line. We found that TP53TG1 overexpression significantly inhibited cell proliferation and induced apoptosis, and TP53TG1 may be a novel anti-oncogenic factor in cervical cancer. Mechanistically, overexpression of TP53TG1 could activate type I interferon signaling pathways and inhibits the expression of genes involved in DNA damage responses. Meanwhile, TP53TG1 could regulate the expression of a large number of RNA binding protein genes thereby potentially affecting the alternative splicing of genes involved in cell proliferation or apoptosis regulation. We also established a ceRNA network to predict the regulatory effect of TP53TG1 on gene expression through miRNA. Our study highlights the essential role of lncRNA TP53TG1 in the development of cervical cancer and suggests the potential regulatory mechanisms.

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2023-03-10 | GSE224301 | GEO

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Project description:Background: Retinal neovascularization (RNV) is a leading cause of blindness worldwide. Long non-coding RNA (lncRNA) and competing endogenous RNA (ceRNA) regulatory networks play vital roles in angiogenesis. The RNA-binding protein galectin-1 (Gal-1) participates in pathological RNV in oxygen-induced retinopathy mouse models. However, the molecular associations between Gal-1 and lncRNAs remain unclear. Herein, we aimed to explore the potential mechanism of action of Gal-1 as an RNA-binding protein. Results: A comprehensive network of Gal-1, ceRNAs, and neovascularization-related genes was constructed based on transcriptome chip data and bioinformatics analysis of human retinal microvascular endothelial cells. We also conducted functional enrichment and pathway enrichment analyses. Fourteen lncRNAs, twenty-nine miRNAs, and eleven differentially expressed angiogenic genes were included in the Gal-1/ceRNA network. WT1-AS, LINC01140, and LUCAT1 were situated at the center of the network. Additionally, several key angiogenic genes, such as apelin, angiomotin, and C-X-C motif chemokine ligand 10, were found to potentionally interact with Gal-1 via the ceRNA axis. Furthermore, Gal-1 may be involved in regulating biological processes related to chemotaxis, chemokine-mediated signaling, the immune response, and the inflammatory response. Conclusions: The Gal-1/ceRNA axis identified in this study may play a vital role in RNV. This study provides a foundation for the continued exploration of therapeutic targets and biomarkers associated with RNV.

2023-06-21 | GSE221037 | GEO

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