The kit measures hsa-miR-31-5p isolated from human blood
Assay format is 96 wells
Standard is synthetic miRNA-based
Components of the kit are provided ready to use, concentrated or dried
Cardiovascular disease, Oncology
MicroRNAs (miRNAs) are small non-coding RNA molecules, approximately 22 nucleotides in length that regulate gene translation through silencing or degradation of target mRNAs. They are involved in multiple biological processes, including differentiation and proliferation, metabolism, hemostasis, apoptosis or inflammation, and in the pathophysiology of many diseases. Numerous studies have suggested circulating miRNAs as promising diagnostic and prognostic biomarkers of many diseases.
miRNA-31, including its mature forms miR-NA-31-3p and miRNA-31-5p, has a dual role, both oncogenic and tumor-suppressing, being disrupted in many human cancers. Aberrant expression of miR-31-5p has been detected in various cancers and plays a significant role in tumorigenesis. Low miR-31-5p expression was present in nasopharyngeal carcinoma tissues and cell lines and acted as a tumor suppressive miRNA and low expression of miR-31-5p was highly correlated with tumor-node-metastasis stage. Serum miR-31-5p levels were significantly different between oral cancer patients and healthy controls and between pre- and postoperative patients. Furthermore, a miR-31-5p mimic enhanced the proliferation of normal epithelial cells, and antagomiR-31-5p inhibited the proliferation of oral cancer cells. miR-31-5p was proven to have oncogenic properties in both colorectal cancer (CRC) cell lines and primary colorectal tumors. In CRC, miR-31-3p and miR-31-5p dysregulation seems to have a particular role in response to treatment with anti-EGFR therapy. miR-31-5p was significantly down-regulated in renal cell carcinoma (RCC) tissues and cell lines compared with paired adjacent normal tissues and normal cell lines. miR-31-5p downregulation was associated with poor prognosis in RCC patients. Overexpression of miR-31-5p inhibited RCC cell proliferation, migration and invasion and cell cycle.
Besides cancer, it was found that miR-31-5p was up-regulated in sera from patients with preeclampsia and in human endothelial cells treated with TNFα. TNFα-mediated induction of miR-31-5p was blocked by an NF-κB inhibitor. It was suggest that NF-κB-responsive miR-31-5p elicits endothelial dysfunction, hypertension, and vascular remodeling via post-transcriptional down-regulation of eNOS and is a molecular risk factor in the pathogenesis and development of preeclampsia.
Summary References (5)
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