Skeletal muscle satellite cells (SCs) play an important role in the repairment and regeneration of damaged muscle. The activation, proliferation, migration, and differentiation of SCs are essential to the response to muscle injury. Up-frameshift 1 (UPF1) is involved in the regulation of many developmental processes. However, the role of UPF1 and its associated regulatory mechanism in SCs are still unclear. Here, we analyzed changes in the transcriptome of porcine SCs with UPF1 knockdown. The results showed that focal adhesion and actin cytoskeleton processes were regulated by UPF1. We also confirmed experimentally that UPF1 promoted SC migration and adhesion by regulating the expression of F-Actin, Vinculin, and several adhesion-related genes. Furthermore, we found that phosphorylated focal adhesion kinase (p-FAK) was down-regulated by UPF1 knockdown. This study identifies the role of UPF1 in regulating SC migration and adhesion and therefore provides new insight into the regulatory mechanism of UPF1 in the process of repairing damaged muscle.

骨骼肌卫星细胞（SCs）在受损肌肉的修复和再生中发挥着重要作用。SCs 的激活、增殖、迁移和分化对于肌肉损伤的反应至关重要。上移码 1 (UPF1) 涉及许多发育过程的调节。然而，UPF1 及其在 SCs 中的相关调控机制的作用仍不清楚。在这里，我们分析了 UPF1 敲低后猪 SCs 转录组的变化。结果表明，粘着斑和肌动蛋白细胞骨架过程受UPF1的调节。我们还通过实验证实，UPF1 通过调节 F-Actin、Vinculin 和几种粘附相关基因的表达来促进 SC 迁移和粘附。此外，我们发现磷酸化粘着斑激酶（p-FAK）被UPF1敲低下调。该研究确定了UPF1在调节SC迁移和粘附中的作用，从而为UPF1在修复受损肌肉过程中的调节机制提供了新的见解。