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Circulating miR 802-5p and miR 194-5p and brain expression of MEF2C as novel biomarkers of breast cancer brain metastasis

ABSTRACT: Circulating miR 802-5p and miR 194-5p and brain expression of MEF2C as novel biomarkers of breast cancer brain metastasis

PROVIDER: PRJNA561379 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10010843.fastq.gz	Fastqsanger.gz
	SRR10010844.fastq.gz	Fastqsanger.gz
	SRR10010845.fastq.gz	Fastqsanger.gz
	SRR10010846.fastq.gz	Fastqsanger.gz
	SRR10010847.fastq.gz	Fastqsanger.gz

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Circulating miR 802-5p and miR 194-5p and brain expression of MEF2C as novel biomarkers of breast cancer brain metastasis

Project description:We hypothesized that circulating miRNAs could work as biomarkers for early detection of breast cancer brain metastasis (BCBM), and their targets could constitute new targets for modulation. We used a mouse model of BCBM and Next-Generation Sequencing to establish the circulating miRNAs alterations along brain metastasis development and performed bioinformatics analysis to identify their targets with relevance in the metastatic process. We additionally analyzed human resected brain metastasis of breast cancer patients for target’s expression validation. In our mouse model, we observed a deregulation of circulating miRNAs profile during BCBM progression, with a downregulation of miR-802-5p and miR-194-5p in plasma prior to brain metastases detection. The transcription factor myocyte enhancer factor 2C (MEF2C), was identified as a target for both miRNAs, and its expression was increasingly observed in malignant cells along brain metastasis development. Its upregulation was also observed in peritumoral astrocytes and in human BCBM. Collectively, downregulation of circulating miR-802-5p and miR-194-5p appear as precocious biomarkers for BCBM and MEF2C emerges as a new player and a potential target for modulation.

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RNA-seq expression analysis of mouse liver treated with locked nucleic acids (LNAs) that inhibit mmu-miR-802-5p and mmu-miR-1948-5p

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Identification of miR-194-5p target genes in gastric cancer

Project description:Increasing studies report that miR-194-5p plays a tumor suppressor role in gastric cancer (GC). Previous studies have revealed that miR-194 inhibited gastric cancer progression through different pathways by affecting the expression level of different target genes. For example, miR-194 have been reported to be able to regulate the expression of FOXM1, NR2F2, BMI1, SDAD1, RBX1, KDM5B, ZEB1 and AKT2 etc. It suggested that miR-194 may play complicated roles in GC. To figure out the mechanism of miR-194' tumor suppressor role in GC, we performed RNA sequencing in two different GC cell lines. Our studies showed that miR-194 tends to regulated target genes by binding on their 3' untranslated regions with either 7-mer-A1 or 7-mer-m8 or 8-mer. Approximately 138 genes were downregulated in both SGC7901 and BGC823 cell lines that transfected with miR-194-5p mimics compared to negative control siRNAs. Most of the downregulated genes have not reported yet.

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Project description:Non-alcoholic fatty liver disease (NAFLD) involves hepatic accumulation of intracellular lipid droplets via incompletely understood processes. Here, we report distinct and cooperative NAFLD roles of LysTTT-5’tRF transfer RNA fragments and microRNA miR-194-5p. Unlike lean animals, dietary-induced NAFLD mice showed concurrent hepatic decrease of both LysTTT-5’tRF and miR-194-5p levels, which were restored following miR-132 antisense oligonucleotide treatment which suppresses hepatic steatosis. Moreover, exposing human-derived Hep G2 cells to oleic acid for 7 days co-suppressed miR-194-5p and LysTTT-5’tRF levels while increasing lipid accumulation. Importantly, transfecting fattened cells with a synthetic LysTTT-5’tRF mimic elevated mRNA levels of the metabolic regulator β-Klotho while decreasing triglyceride amounts by 30% within 24 hours. In contradistinction, antisense suppression of miR-194-5p induced accumulation of its novel target, the NAFLD-implicated lipid droplet-coating PLIN2 protein. Further, two out of 15 steatosis-alleviating screened drug-repurposing compounds, Danazol and Latanoprost, elevated miR-194-5p or LysTTT-5’tRF levels. The different yet complementary roles of miR-194-5p and LysTTT-5’tRF offer new insights into the complex roles of small non-coding RNAs and the multiple pathways involved in NAFLD pathogenesis.

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