1,823,999 research outputs found
Expression analysis of exosomal miRNA-330-3p in RA patients.
No full text(A) Relative expression level miRNA-330-3p in RA patients vs controls. (B) Association of relative expression of miRNA-330-3p with demographic/pathological parameters of RA patients such as age, gender, anti-CCP level, ESR level, and CRP level. (C) ROC curve analysis of miRNA-330-3p in RA disease. Level of significance p<0.05.</p
<i>Srpr</i> is a direct target of miR-330-5p in mouse keratinocyte.
No full text(A) Location of the binding site for miR-330-5p in 3’UTR of Srpr mRNA. Deletion is depicted in red hyphen. (B) Dual Luciferase assay showed that miR-330-5p directly inhibited the luciferase activity by targeting the binding site in Srpr 3’UTR. However, luciferase activity did not change significantly when cells were co-transfected with the deletion mutant lacking the miR-330-5p-binding site and the miR-330-5p. (C-E) Mir-330-5p suppressed the proliferation of PAM212 cells through inhibition of SRPR expression. (C) Real-time quantitative PCR showed that cotransfection of miR-330-5p and the full length SRPR-cDNA (Srpr CDS) was able to abolish the decreased expression of Srpr by miR-330-5p alone. (D) Proliferation of PAM212 cells was decreased by miR-330-5p. Co-transfection with the Srpr CDS construct rescued inhibition of cell proliferation by miR-330-5p. (E) Relative viable cells were measured at 72 h after transfection. (B-E) Results are the average of three independent experiments. **PP<0.001. NS = no significance.</p
LIPIcs, Volume 330, SAND 2025, Complete Volume
No full textLIPIcs, Volume 330, SAND 2025, Complete Volum
Supplementary Material for: Clinical significance of microRNA-330-3p in plasma level for acute cerebral infarction
No full textIntroduction: The present study was to investigate the clinical role of miR-330-3p in acute cerebral infarction (ACI), including its diagnostic and prognostic potential. Preliminary exploration of its target genes was archived by bioinformatics analysis.
Methods: miR-330-3p in plasma of the patients with ACI and controls were quantified by real-time quantitative PCR. The one-month prognosis of the ACI patients was evaluated by the Glasgow outcome scale (GOS). The correlation between the plasma levels of miR-330-3p and the GOS scores was tested by Pearson correlation analysis. The receiver operating characteristic (ROC) curves were established based on the expression level of miR-330-3p in different groups. The miR-330-3p-targeting genes were analyzed using Venn diagram, protein-protein interaction network, and Gene Ontology enrichment analysis.
Results: MiR-330-3p was significantly increased in the plasma of ACI patients compared with that in healthy controls, and ROC curve revealed its diagnostic value for ACI. miR-330-3p was significantly increased in the plasma of patients with poor one-month prognosis compared with those with good one-month prognosis. MiR-330-3p expression was negatively correlated with GOS score, suggesting its potential to predict the one-month prognosis for ACI. One-year survival analysis revealed surviving patients had lower levels of miR-330-3p than the deceased. miR-330-3p was proven to predict the death of patients with ACI. The miR-330-3p-targeting genes were associated with synapse-related Gene Ontology terms.
Conclusion: MiR-330-3p was upregulated in the plasma of patients with ACI, making it a promising diagnostic and prognostic marker for patients with ACI. MiR-330-3p could facilitate synaptic plasticity following cerebral infarction
Additional file 1: of Silencing microRNA-330-5p increases MMP1 expression and promotes an invasive phenotype in oesophageal adenocarcinoma
No full textTable S1. Transcriptome gene expression analysis log2 fold change in the OE33 miRZIP-330-5p SC cell line and predicted binding sites for miR-330-3p and miR-330-5p. (DOCX 17 kb
MiR-330-5p regulates <i>Srpr</i> expression in mouse epidermal keratinocyte.
No full text(A) Targetscan algorithm predicted that a conserved binding sequence of miR-330-5p was present in the 3’ UTR of Srpr mRNA. (B) Real-time quantitative PCR was performed to validate the result of previous study using the same total RNA used for microarray analysis. (C) MiR-330-5p down-regulated the Srpr expression at 25nM, 50nM and 100nM mimic transfected PAM212 cells. The data was normalized against Gapdh expression. (D) Western blot analysis also revealed that SRPR protein level was decreased at 50nM and 100nM miR-330-5p mimic transfected PAM212 cells in comparison to the control. β-actin was used as a loading control. (E) Quantitative analysis of western blot using ImageJ software. The SRPR band intensity was normalized against GAPDH expression. (F) Srpr expression was significantly increased by inhibition of miR-330-5p. (B-F) Results are the average of three independent experiments. *PPP<0.001.</p
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