Hsa-miR-144-3p is down-regulated in serum from drug-naïve and advanced Parkinson’s disease patients.
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ABSTRACT:
PROVIDER: PRJNA747006 | ENA |
REPOSITORIES: ENA
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Project description:Advanced age represents one of the major risk factors for Parkinson’s Disease. Recent studies posit a role for microRNAs in Parkinson’s Disease and it is well established that microRNAs are remodelled during ageing, but the relationship between the two processes have not been clarified yet. The aim of the present study is to unravel the relevance of microRNAs as biomarkers of Parkinson’s Disease within the ageing framework. We used Next Generation Sequencing to profile serum microRNAs from samples informative for Parkinson’s Disease (recently diagnosed, drug-naïve Parkinson’s Disease patients) and healthy ageing (centenarians) plus healthy controls age-matched with Parkinson’s Disease patients. Potential candidates, emerging from the combination of differential expression and network analyses, were further validated in an independent cohort including both drug-naïve and advanced Parkinson’s Disease patients together with healthy siblings of Parkinson’s Disease patients at higher genetic risk for Parkinson’s Disease. While we did not find evidences of microRNAs co-regulated in Parkinson’s Disease and ageing, we report that hsa-miR-144-3p is consistently down-regulated in early and advanced Parkinson’s Disease and in Parkinson’s Disease siblings. Interestingly, functional analysis revealed that hsa-miR-144-3p is involved in the regulation of coagulation, a process known to be altered in Parkinson’s Disease. Our results consistently show the down-regulation of hsa-mir144-3p in early and advanced Parkinson’s Disease, robustly confirmed across a variety of analytical and experimental analyses. These results are promising, and additional research is needed to unveil the functional details of its relevance and involvement in Parkinson’s Disease.
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Project description:miRNAs are small noncoding RNA molecules that play an important role in post-transcriptional regulation of gene expression. Length and/or sequence variants of the same miRNA are termed isomiRs. While most isomiRs are functionally redundant compared to their canonical counterparts, so-called 5âisomiRs exhibit a shifted 5â end and therefore a shifted seed sequence resulting in a different target spectrum. However, not much is known about the functional relevance of these isoforms. Analysis of miRNA-seq data from breast cancer cell lines identified six pairs of highly expressed miRNAs and associated 5âisomiRs. Among them, hsa-miR-140-3p was of particular interest because its 5âisomiR showed higher expression compared to the canonical miRNA annotated in miRbase. This miRNA has previously been shown to control stemness of breast cancer cells. MiRNAseq data of breast cancer patients (TCGA dataset) showed that both the canonical hsa-miR-140-3p and its 5âisomiR-140-3p were highly expressed in patients compared to normal breast tissue. In the current work, we present the functional characterization of 5âisomiR-140-3p and the cellular phenotypes associated with its overexpression in MCF10A and MDA-MB-231 cell lines in comparison to the canonical hsa-miR-140-3p. Contrary to the effect of the canonical hsa miR 140-3p, overexpression of the 5âisomiR-140-3p led to a decrease in cell viability. The latter observation was supported by cell cycle analysis, where the 5âisomiR-140-3p but not the hsa-miR-140-3p caused cell cycle arrest in G0/G1-phase. Additionally, 5âismoiR-140-3p overexpression was found to cause a decrease in cell migration in MCF10A cells. We identified three novel direct target genes of the 5â isomiR-140-3p; COL4A1, ITGA6 and MARCKSL1. Finally, we have shown that knocking down these genes partially phenocopied the effects of the 5âisomiR-140-4p overexpression, where COL4A1 and ITGA6 knockdown led to reduced cell viability and cell cycle arrest, while MARCKSL1 knockdown resulted in a decrease in the migratory potential of cells. In summary, this work presents evidence that there is a functional synergy between the canonical hsa-miR-140-3p and the newly identified 5âisomiR-140-3p in suppressing growth and progression of breast cancer by simultaneously targeting genes related to differentiation, proliferation, and migration. With this array, we aimed to address the question which genes are regulated by either of the two forms of the miRNA. Samples were measured in one biological replicate of cells transfected with mimic-ctrl1 and mimic-ctrl2 (Dharmacon) as control samples and two biological replicates of cells transfected with hsa-miR-140-3p and 5'isomiR-140-3p (Exiqon) in 30nM concentration using Lipofectamin 2000 as transfection reagent.
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