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.
miR-499a-5p was upregulated in both highly metastatic lung cancer cell line and their exosomes. Overexpression of miR-499a-5p promoted cell proliferation, migration and epithelial-mesenchymal transition (EMT). Inhibition of miR-499a-5p by antagomirs administration restrained tumor growth in vivo. Serum level expression of miR-499a-5p in patients with pancreatic cancer was significantly higher than that in both the benign and healthy control groups. But there was no difference in serum miR-499a-5p level between the benign control group and the healthy control group. miR-499a-5p was significantly downregulated in degenerative tissues of the human nucleus pulposus (NP) compared with healthy tissues. Knockdown of miR-499a-5p promoted NP cell (NPC) apoptosis, stimulated caspase activation, enhanced MMP3 and MMP13 expression, and downregulated aggrecan and type II collagen. miR-499a-5p which exerted a tumour-spressive function was significantly downregulated in glioma cells. miR-499a-5p was also found to be down-regulated in many tumours (e.g. oral squamous cell carcinoma, osteosarcoma and cervical cancer.
miR-499a-5p plays a role in the damage of cardiomyocytes induced by hypoxia/reoxygenation. The activity of lactate dehydrogenase (LDH), apoptosis rate and the expression of miR-499a-5p and cluster of differentiation 38 (CD38) in hypoxia-reoxygenation model cells were detected.
Apoptosis, the activity of LDH was detected after overexpression of miR-499a-5p or silencing of CD38 in H9c2 cells. miR-499a-5p could relieve the injury of cardiomyocytes induced by hypoxia/reoxygenation via targeting CD38. miR-499a-5p overexpression promotes the cardiomyogenic differentiation of hBM-MSCs.