Tilianin improves cognition in a vascular dementia rodent model by targeting miR-193b-3p/CaM- and miR-152-3p/CaMKIIα-mediated inflammatory and apoptotic pathways
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ABSTRACT:
PROVIDER: PRJNA950046 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24006375_1.fastq.gz | Fastqsanger.gz | |||
| SRR24006375_2.fastq.gz | Fastqsanger.gz | |||
| SRR24006376_1.fastq.gz | Fastqsanger.gz | |||
| SRR24006376_2.fastq.gz | Fastqsanger.gz | |||
| SRR24006377_1.fastq.gz | Fastqsanger.gz |
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Project description:The mouse mSCC-20 cell line was transfected with 5nM of mmu-pre-miR-193b-3p, pre-miR-365a-3p or pre-miR-NC1. Total RNAs were extracted 30 h after transfection and hybridized on microarrays. One color experiment with 3 experimental conditions : miR-NC1- (n=4), miR-193b-3p- (n=2) and miR-365-3p- (n=2) transfected cells, corresponding to a total of 8 samples.
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Project description:Meningiomas are common intracranial tumors in adults. Abnormal miRNA expression plays a role in their pathogenesis. Change in miRNA expression level can be caused by impaired epigenetic regulation of miRNA-encoding genes. We found genomic region covering MIR193B gene as DNA hypermethylated in meningiomas based on analysis of genome-wide methylation (HM450k Illumina arrays). Hypermethylation of MIR193B was as also confirmed by bisulfite pyrosequencing. Both hsa-miR-193b-3p and hsa-miR-193b-5p are downregulated in meningiomas as found with qRT-PCR. Lower expression of hsa-miR-193b-3p and higher MIR193b methylation was observed in WHO GII/GIII as compared to GI meningiomas. 3’UTR of CCND1 mRNA was identified as target of hsa-miR-193b-3p as further validated with luciferase reporter assay in IOMM-Lee meningioma cells. IOMM-Lee cells transfected with hsa-miR-193b-3p mimic showed decreased cyclin D1 level and lower cell viability and proliferation, confirming suppressive nature of this miRNA. Cyclin D1 protein expression (immunoreactivity) was higher in atypical than in benign meningiomas, accordingly to observation of lower hsa-miR-193b-3p level in GII tumors. The commonly observed hypermethylation of MIR193B in meningiomas apparently contributes to downregulation of hsa-miR-193b-3p. Since hsa-miR-193b-3p regulates proliferation of meningioma cells through negative regulation of cyclin D1 expression, it seems to be an important tumor suppressor in meningiomas.
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Project description:The mouse mSCC-20 cell line was transfected with 5nM of mmu-pre-miR-193b-3p, pre-miR-365a-3p or pre-miR-NC1. Total RNAs were extracted 30 h after transfection and hybridized on microarrays.
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Project description:MicroRNAs (miRNAs) have important roles in gene regulation. Dysregulation of miRNAs has been associated with tumorigenesis. Recent studies suggest miR-193b is a tumor suppressor gene. In a previous study, we reported that miR-193b represses cell proliferation and regulates cyclin D1 (CCND1) in melanoma. Now we demonstrate that miR-193b regulates myeloid cell leukemia sequence 1 (Mcl-1) in melanoma cells. miRNA microarray profiling revealed the miR-193b level in malignant melanomas was significantly downregulated compared to benign nevi, while a tissue microarray demonstrated overexpression of Mcl-1 in malignant melanoma. The Mcl-1 expressions were inversely correlated with the miR-193b levels in melanoma tissue samples, suggesting a potential regulatory role of miR-193b. Overexpression of miR-193b repressed Mcl-1 in melanoma cell lines. It is well known that Mcl-1 knockdown confers cell sensitivity to ABT-737, a small molecular inhibitor of Bcl-2, Bcl-XL and Bcl-w. We found miR-193b, through repressing Mcl-1 expression, could also sensitize melanoma cells that were refractory to ABT-737. Furthermore, miR-193b directly regulates Mcl-1 by targeting the 3â untranslated region (3âUTR) of Mcl-1 mRNA. Interestingly, miR-193b may recognize sequences on the 3âUTR that do not base pair with its seed region. In conclusion, our study suggests the downregulation of miR-193b could be an early event during melanoma progression, and demonstrates miR-193b directly regulates Mcl-1 by targeting both seed and seedless sequences of the 3â UTR. 15 primary melanoma samples, 8 metastatic melanomas and 8 benign nevi samples were profiled on Agilent miRNA array platform
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