MicroRNA (miR) deregulation is frequently seen in colon cancer. In this study, we sought to investigate biological effects of miR-193a on colon cancer and its underlying mechanism. Microarray analysis was conducted to obtain the differentially expressed miRs and their target genes in colon cancer. Bone-marrow derived mesenchymal stem cells (MSCs) and extracellular vesicles (EVs) were obtained. The functional roles of miR-193a and FAK in colon cancer were determined using loss- and gain-function experiments. The cell proliferation, and migration and invasion were evaluated by CCK-8 and Transwell assay respectively. Dual-luciferase reporter assay was performed to confirm the targeting relationship between miR-193a and FAK. Furthermore, in vivo experiment was conducted to test the roles of EV miR-193a in colon cancer growth, followed by determination of PCNA, MMP-2, and MMP-9 protein expression using Western blot analysis. MiR-193a was downregulated, whereas FAK was upregulated in colon cancer. MiR-193a upregulation or FAK downregulation inhibited proliferation, migration and invasion of colon cancer cells. miR-193a could downregulate FAK. Upregulation of EV miR-193a was observed to impede proliferation, migration and invasion of colon cancer cells in vitro and in vivo, accompanied by decreased PCNA, MMP-2, and MMP-9 expression. In summary, EV miR-193a derived from MSCs impeded colon cancer progression by targeting FAK, thus suggesting a new potential strategy for colon cancer treatment.

MicroRNA（miR）解除管制在结肠癌中经常出现。在这项研究中，我们试图研究miR-193a对结肠癌的生物学作用及其潜在机制。进行微阵列分析以获得结肠癌中差异表达的miR及其靶基因。获得了骨髓来源的间充质干细胞（MSCs）和细胞外囊泡（EVs）。使用丢失和获得功能实验确定了miR-193a和FAK在结肠癌中的功能。分别通过CCK-8和Transwell法评估细胞的增殖，迁移和侵袭。进行双荧光素酶报告基因测定以证实miR-193a和FAK之间的靶向关系。此外，体内进行了实验以测试EV miR-193a在结肠癌生长中的作用，然后使用蛋白质印迹分析确定PCNA，MMP-2和MMP-9蛋白的表达。在结肠癌中，MiR-193a被下调，而FAK被上调。MiR-193a上调或FAK下调抑制了结肠癌细胞的增殖，迁移和侵袭。miR-193a可能下调FAK。观察到EV miR-193a的上调可在体外和体内阻止结肠癌细胞的增殖，迁移和侵袭，并伴有PCNA，MMP-2和MMP-9表达降低。总之，源自MSC的EV miR-193a通过靶向FAK来阻止结肠癌的进展，从而提示了结肠癌治疗的新的潜在策略。