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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.

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