MicroRNA‐543 (miR‐543) has been found to play a suppressive role in various human cancers in many studies, whereas the specific functions of miR‐543 in muscle development remain poorly understood. Here, we found that the expression of miR‐543 was high in skeletal muscle and increased during the differentiation of C2C12 cells. Overexpression of miR‐543 repressed C2C12 cell proliferation and promoted differentiation, while knockdown of miR‐543 expression produced the opposite results. During myogenesis, we predicted and verified that Krüppel‐like factor 6 (KLF6), a suppressor of multiple tumor cells, was a target gene of miR‐543. Then, miR‐543 was found to specifically target KLF6 and repress its expression. Besides this, knockdown of KLF6 promoted the differentiation but inhibited the proliferation of C2C12 cells. Si‐KLF6 can rescue the influence of miR‐543 inhibitor on C2C12 cell differentiation. Our results indicate a new regulatory mechanism of miR‐543 on KLF6 expression and suggest the possibility of using the miR‐543/KLF6 pathway as a potential target for studying myogenesis.

中文翻译：

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MiR-543 通过靶向 KLF6 调节 C2C12 细胞的成肌细胞增殖和分化。

许多研究发现 MicroRNA-543 (miR-543) 在多种人类癌症中发挥抑制作用，但 miR-543 在肌肉发育中的具体功能仍知之甚少。在这里，我们发现 miR-543 在骨骼肌中表达较高，并且在 C2C12 细胞分化过程中表达增加。miR-543 的过度表达抑制 C2C12 细胞增殖并促进分化，而 miR-543 表达的敲低则产生相反的结果。在肌生成过程中，我们预测并验证了多种肿瘤细胞的抑制因子 Krüppel 样因子 6 ( KLF6 ) 是 miR-543 的靶基因。然后，发现 miR-543 特异性靶向KLF6并抑制其表达。除此之外，KLF6的敲低促进了C2C12细胞的分化但抑制了增殖。Si-KLF6可以挽救miR-543抑制剂对C2C12细胞分化的影响。我们的结果表明 miR-543 对KLF6表达的新调节机制，并表明使用 miR-543/ KLF6途径作为研究肌发生的潜在靶点的可能性。