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Apart from the experimental studies in vitro already mentioned, there are also many in vivo experimental studies that demonstrate the role of miRNA in the treatment of MM. Ueno et al. (2014) injected adenovirus-carried miR-34b/c into explants of MM tissues from mice and found that the expression of miR-34b/c in tumor cells increased. When compared with the lentivirus-carried luciferase treatment, the volume of tumor did not change for six to ten days after injection, which indicated that miR-34b/c has a certain inhibitory effect on tumor growth. Another study transplanted tumors in nude mice, and then injected into these mice, intravenously, micro cells containing miR-16 analogues. It was found that the degree of inhibition of tumor growth became more obvious as the dose increased; and DNA fragment analysis found that miR-16 analogues also damaged intracellular DNA. When MSTO-211H or MM 05 cell line is transfected with miR-16 analogue, the sensitivity of tumor cells to chemotherapy drugs increases and the efficacy of these drugs is enhanced (Reid et al. 2013). Cioce et al. (2014) inoculated the experimental mice with MSTO-211H. The results showed that eight out of eight mice in the positive control group that were not transfected with miR-145 analogues had solid tumors, while only two out of eight mice in the experimental group that were transfected with miR-145 analogues had tumors; and the tumor volume in the experimental group was significantly smaller than in the positive control group. These experimental results on animals provide more powerful evidence for the usefulness of miRNA in the treatment of MM.

miRNA is able not only to regulate cell cycle, proliferation, clone formation, migration, invasion ability, and apoptosis or inhibit the growth of explant tumors, but also to improve the sensitivity of tumor cells to traditional radiotherapy by regulating the expression level of some miRNAs in cells. Increased expression of miR-34b/c in tumor cells can destroy DNA double-strand damage repair and inhibit the expression of tumor cell growth-related proteins. It can also enhance the sensitivity of MM cells to radiation, which indicates that the combination of increased expression level of miR-34b/c in cells and radiotherapy may be used for the treatment of MM (Maki et al. 2012). At present, on the basis of this research, the application of miRNA to the treatment of MM produces the following three ideas. First, miRNA antagonist is used to inhibit the effect of carcinogenic miRNA, block endogenous miRNA from being processed by RISC, or lead to the degradation of endogenous miRNA. The second idea is to enhance the expression level of the endogenous tumor suppressor miRNA and inhibit the expression of its target proto-oncogene (Benjamin et al. 2010). The third idea is to use the artificial miRNA (amiRNA) expression vector that targets genes related to the malignant tumor phenotype. These methods could become a new way of treating MM, namely by interfering with the changes in miRNA expression level related to the occurrence and development of the tumor.