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The oncogenic microRNA miR-222 promotes human LINE-1 retrotransposition

ABSTRACT: The oncogenic microRNA miR-222 promotes human LINE-1 retrotransposition

PROVIDER: PRJNA1141495 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30033225.fastq.gz	Fastqsanger.gz
	SRR30033226.fastq.gz	Fastqsanger.gz
	SRR30033227.fastq.gz	Fastqsanger.gz
	SRR30033228.fastq.gz	Fastqsanger.gz
	SRR30033229.fastq.gz	Fastqsanger.gz

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The oncogenic microRNA miR-222 promotes human LINE-1 retrotransposition

Project description:The Long Interspersed Element-1 (LINE-1) contributes significantly to carcinogenesis and to tumor heterogeneity in many cancer types, including hepatocellular carcinoma (HCC), by its autonomous retrotransposition (RTP) and by its ability to retrotranspose some non-autonomous transposable elements. Previously, multiple proteins and a few microRNAs (miRs) were described as regulators of LINE-1 RTP. Here, we demonstrate that miR-222, which is oncogenic in HCC, promotes LINE-1 RTP in human HCC and some other cell lines in vitro, and that both miR-222-3p and miR-222-5p activate LINE-1 RTP in a cell type-specific manner. We generated miR-222-knockout mutants of the Huh7 and FLC4 HCC cell lines, and performed RNA-seq analysis of Huh7/miR-222-knockout cells and global proteomics analysis of both Huh7 and FLC4 miR-222-knockout mutants. We demonstrate that miR-222 decreases let-7c expression in both Huh7 and FLC4 cells, and that this decrease contributes to promotion of LINE-1 RTP by miR-222 in Huh7 cells.

2025-06-16 | GSE273369 | GEO

microRNA-222 Attenuates Mitochondrial Dysfunction Induced by Transmissible Gastroenteritis Virus via Targeting Thrombospondin-1 and Inhibiting Cluster of Differentiation 47

Project description:Transmissible gastroenteritis virus (TGEV) is a member of Coronaviridae family. Our previous research showed that TGEV infection could induce mitochondrial dysfunction and up-regulat miR-222 level. Therefore, we presumed that miR-222 might be implicated in regulating mitochondrial dysfunction induced by TGEV infection. To verify the hypothesis, the effect of miR-222 on mitochondrial dysfunction was detected and showed that miR-222 attenuated TGEV-induced mitochondrial dysfunction. To investigate the underlying molecular mechanism of miR-222 in TGEV-induced mitochondrial dysfunction, a quantitative proteomic analysis of PK-15 cells that were transfected with miR-222 mimics and infected with TGEV was performed. In total, 4151 proteins were quantified and 100 differentially expressed proteins were obtained (57 up-regulated, 43 down-regulated), among which thrombospondin-1 (THBS1) and cluster of differentiation 47 (CD47) were down-regulated. THBS1 was identified as the target of miR-222. Knockdown of THBS1 and CD47 increased mitochondrial Ca2+ level and decreased mitochondrial membrane potential (MMP) level. Together, our data establish a significant role of miR-222 in regulating mitochondrial dysfunction in response to TGEV infection.

2018-12-19 | PXD010927 | Pride

Gene expression profiling of MCF10A (miR-221/222 vs control)

Project description:Analysis of gene expression of MCF10A to identify the targets of miR-221 and miR-222 Keywords: MCF10, miR-221, miR-222

2011-06-14 | GSE29327 | GEO

Gene expression profiling of MCF10A (miR-221/222 vs control)

Project description:Analysis of gene expression of MCF10A to identify the targets of miR-221 and miR-222 Keywords: MCF10, miR-221, miR-222 RNA profiles of human MCF10A cell line

2011-06-14 | E-GEOD-29327 | biostudies-arrayexpress

miR-221/222 drive synovial fibroblast expansion and pathogenesis of TNF-mediated arthritis

Project description:MicroRNAs (miRNAs) constitute fine tuners of gene expression and are implicated in a variety of diseases spanning from inflammation to cancer. miRNA expression is deregulated in rheumatoid arthritis (RA), however, their specific role in key arthritogenic cells such as the synovial fibroblast (SF) remains elusive. We have shown in the past that the expression of the miR-221/222 cluster is upregulated in RA SFs. Here, we demonstrate that miR-221/222 activation is downstream of major inflammatory cytokines, such as TNF and IL-1β, which promote miR-221/222 expression independently. miR-221/222 expression in SFs from the huTNFtg mouse model of arthritis correlates with disease progression. Targeted transgenic overexpression of miR-221/222 in SFs of the huTNFtg mouse model led to further expansion of synovial fibroblasts and disease exacerbation. miR-221/222 overexpression altered the transcriptional profile of SFs igniting pathways involved in cell cycle progression and ECM regulation. Validated targets of miR-221/222 included p27 and p57 cell cycle inhibitors, as well as Smarca1 (a chromatin remodeling component). In contrast, complete genetic ablation of miR-221/222 in arthritic mice led to decreased proliferation of fibroblasts, reduced synovial expansion and attenuated disease. scATAC-seq data analysis revealed increased miR-221/222 gene activity in the pathogenic and activated clusters of the intermediate and lining compartment. Taken together, our results establish an SF-specific pathogenic role of the miR-221/222 cluster in arthritis and suggest that its therapeutic targeting in specific subpopulations should inform the design of novel fibroblast-targeted therapies for human disease.

2022-12-16 | GSE210887 | GEO

The SWI/SNF complex regulates the expression of miR-222, a tumor suppressor microRNA in lung adenocarcinoma

Project description:Mammalian SWI/SNF complexes are considered as key epigenetic regulators and they are recurrently mutated in many types of cancer. Most of the studies of these chromatin remodeling complexes are focused on their role in regulating protein-coding genes. However, here we show that the SWI/SNF complex is able to control the expression of microRNAs. We used a SMARCA4-deficient model of lung adenocarcinoma where we could track changes of the miRNome upon SMARCA4 restoration. We found that exogenous SMARCA4 was successfully incorporated into endogenous SWI/SNF complexes and that these SMARCA4-SWI/SNF complexes induced significant changes in the expression of cancer-related microRNAs. The most significantly dysregulated miRNA was miR-222, whose expression was promoted by SMARCA4-SWI/SNF complexes but not by SMARCA2-SWI/SNF complexes via their direct binding to a miR-222 enhancer region. Importantly, miR-222 expression decreased cell viability and impaired cell clonogenicity, phenocopying the tumor-suppressor role of the SMARCA4-SWI/SNF complex in lung cancer. Finally, we showed that the miR-222 enhancer does not interact with any cancer-related protein-coding genes, supporting that its tumor suppressor effect may be exerted via miR-222. Overall, this study highlights the relevant role of the SWI/SNF complex in regulating the expression of the non-coding genome.

2021-07-20 | GSE167140 | GEO

Identification of genes differentially expressed in lung cancer cells after the transfection of miR-221 or miR-222.

Project description:To evaluate involvement of miR-221 and miR-222 in lung cancer, we investigated the effects of miR-221 and miR-222 overexpression on six lung cancer cell lines as well as one immortalized normal human bronchial epithelial cell line. Two cell lines, H3255 and H1299 with no replicates were studied. Cells were transfected with miR-221, miR-222, or miR control. Microarray analysis was done to identify genes differentially expressed in lung cancer cells after the transfection of miR-221 or miR-222.

2015-05-22 | E-GEOD-57676 | biostudies-arrayexpress

Identification of genes differentially expressed in lung cancer cells after the transfection of miR-221 or miR-222.

2015-05-22 | GSE57676 | GEO

miR-222 regulation of the tolerized LPS response

Project description:The purpose of this study is to determine the effect miR-221/222 have on LPS-induced gene expression in macrophages.

2018-07-05 | GSE89918 | GEO

Genome-wide miRNA profile of MCF7 cells overexpressing wild-type and mutant miR-222

Project description:MCF7 cells were infected with retrovirus to overexpress wild-type and mutant miR-222 Measure miRNA expression level in MCF7 cells after overexpressing wild-type and mutant miR-222

2015-02-05 | E-GEOD-64363 | biostudies-arrayexpress

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