The kit measures hsa-miR-324-5p 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
Research topic
Cardiovascular disease, Oncology, Others
Summary
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 pathophysiology of many diseases. Numerous studies have suggested circulating miRNAs as promising diagnostic and prognostic biomarkers of many diseases.
miR-324-5p is located on chromosome 17p and exhibits diverse functions in different types of cancer. It was demonstrated that miR-324-5p was upregulated in colon cancer and downregulated in hepatocellular carcinoma and osteosarcoma. In medulloblastoma, miR-324-5p was found to act as a tumour suppressor by inhibiting hedgehog signalling components Smo and Gli1. Another study reported that the expression of miR-324-5p was decreased in multiple myeloma (MM), especially in del(17p) multiple myeloma and that it was essential for activated hedgehog signalling. Moreover, miR-324-5p potentiated the anti-MM efficacy of bortezomib through regulating the activities of multidrug-resistance proteins and the expression of Bcl-2 family genes. Conversely, another study indicated a significant upregulation of miR-324-5p and -3p in lung cancer cells. The results revealed that miR-324-5p and -3p promoted proliferation of lung cancer cells, but only miR-324-5p accelerated the invasion of lung cancer cells. The upregulation of miR-324-5p has also been reported in bladder cancer and urinary level of miR-324-5p correlated with its expression level in tumour tissues.
Besides cancer, miR-324-5p regulates osteogenesis in human mesenchymal stem cells (MSCs) and in mouse C3H10T1/2 cells. An increase in miR-324-5p expression was shown in osteoarthritis cartilage.
It was also published that miR-324-5p might be a potential therapeutic target for myocardial infarction. MiR-324-5p inhibits mitochondrial fission, apoptosis and myocardial infarction through downregulating Mtfr1.
Summary References (9)
References to miR-324-5p
Tang, Bo, et al. "MicroRNA‐324‐5p regulates stemness, pathogenesis and sensitivity to bortezomib in multiple myeloma cells by targeting hedgehog signaling." International journal of cancer 142.1 (2018): 109-120.
Chen, Yuan, et al. "Dysregulation of the miR-324-5p-CUEDC2 axis leads to macrophage dysfunction and is associated with colon cancer." Cell reports 7.6 (2014): 1982-1993.
Cao, Liangqi, et al. "MiR-324-5p suppresses hepatocellular carcinoma cell invasion by counteracting ECM degradation through post-transcriptionally downregulating ETS1 and SP1." PLoS One 10.7 (2015): e0133074.
Dai, N., et al. "Alteration of the microRNA expression profile in human osteosarcoma cells transfected with APE1 siRNA." Neoplasma 60.4 (2013): 384-394.
Ferretti, Elisabetta, et al. "Concerted microRNA control of Hedgehog signalling in cerebellar neuronal progenitor and tumour cells." The EMBO journal 27.19 (2008): 2616-2627.
Lin, Min Hsi, et al. "Comprehensive identification of microRNA arm selection preference in lung cancer: miR 324 5p and 3p serve oncogenic functions in lung cancer." Oncology letters 15.6 (2018): 9818-9826
Eissa, Sanaa, et al. "Measurement of Urinary Level of a Specific Competing endogenous RNA network (FOS and RCAN mRNA/miR-324-5p, miR-4738-3p,/lncRNA miR-497-HG) Enables Diagnosis of Bladder Cancer." Urologic Oncology: Seminars and Original Investigations. Elsevier, 2019.
Woods, Steven, et al. "miR-324-5p is up regulated in end-stage osteoarthritis and regulates Indian Hedgehog signalling by differing mechanisms in human and mouse." Matrix Biology 77 (2019): 87-100.
Wang, K., et al. "NFAT4-dependent miR-324-5p regulates mitochondrial morphology and cardiomyocyte cell death by targeting Mtfr1." Cell death & disease 6.12 (2015): e2007.
