SUMOylation is one of the post-translational modifications that involves the covalent attachment of the small ubiquitin-like modifier (SUMO) to the substrate. SUMOylation regulates multiple biological processes, including myoblast proliferation, differentiation, and apoptosis. 2-D08 is a synthetically available flavone, which acts as a potent cell-permeable SUMOylation inhibitor. Its mechanism of action involves preventing the transfer of SUMO from the E2 thioester to the substrate without influencing SUMO-activating enzyme E1 (SAE-1/2) or E2 Ubc9-SUMO thioester formation. However, both the effects and mechanisms of 2-D08 on C2C12 myoblast cells remain unclear. In the present study, we found that treatment with 2-D08 inhibits C2C12 cell proliferation and differentiation. We confirmed that 2-D08 significantly hampers the viability of C2C12 cells. Additionally, it inhibited myogenic differentiation, decreasing myosin heavy chain (MHC), MyoD, and myogenin expression. Furthermore, we confirmed that 2-D08-mediated anti-myogenic effects impair myoblast differentiation and myotube formation, reducing the number of MHC-positive C2C12 cells. In addition, we found that 2-D08 induces the activation of ErK1/2 and the degradation of MyoD and myogenin in C2C12 cells. Taken together, these results indicated that 2-D08 treatment results in the deregulated proliferation and differentiation of myoblasts. However, further research is needed to investigate the long-term effects of 2-D08 on skeletal muscles.

SUMOylation 是一种翻译后修饰，它涉及小泛素样修饰剂 (SUMO) 与底物的共价连接。SUMOylation 调节多种生物学过程，包括成肌细胞增殖、分化和凋亡。2-D08 是一种合成可用的黄酮，可作为有效的细胞渗透性 SUMOylation 抑制剂。其作用机制包括防止 SUMO 从 E2 硫酯转移到底物，而不影响 SUMO 活化酶 E1 (SAE-1/2) 或 E2 Ubc9-SUMO 硫酯的形成。然而，2-D08对C2C12成肌细胞的作用和机制仍不清楚。在本研究中，我们发现用 2-D08 处理可抑制 C2C12 细胞增殖和分化。我们证实 2-D08 显着阻碍 C2C12 细胞的活力。此外，它还抑制肌原性分化，降低肌球蛋白重链 (MHC)、MyoD 和肌细胞生成素的表达。此外，我们证实 2-D08 介导的抗生肌作用会损害成肌细胞分化和肌管形成，从而减少 MHC 阳性 C2C12 细胞的数量。此外，我们发现 2-D08 在 C2C12 细胞中诱导 ErK1/2 的激活以及 MyoD 和肌细胞生成素的降解。总之，这些结果表明2-D08处理导致成肌细胞增殖和分化失调。然而，需要进一步研究来调查 2-D08 对骨骼肌的长期影响。我们证实 2-D08 介导的抗肌生成作用会损害成肌细胞分化和肌管形成，从而减少 MHC 阳性 C2C12 细胞的数量。此外，我们发现 2-D08 在 C2C12 细胞中诱导 ErK1/2 的激活以及 MyoD 和肌细胞生成素的降解。总之，这些结果表明2-D08处理导致成肌细胞增殖和分化失调。然而，需要进一步研究来调查 2-D08 对骨骼肌的长期影响。我们证实 2-D08 介导的抗肌生成作用会损害成肌细胞分化和肌管形成，从而减少 MHC 阳性 C2C12 细胞的数量。此外，我们发现 2-D08 在 C2C12 细胞中诱导 ErK1/2 的激活以及 MyoD 和肌细胞生成素的降解。总之，这些结果表明2-D08处理导致成肌细胞增殖和分化失调。然而，需要进一步研究来调查 2-D08 对骨骼肌的长期影响。这些结果表明，2-D08 处理导致成肌细胞增殖和分化失调。然而，需要进一步研究来调查 2-D08 对骨骼肌的长期影响。这些结果表明，2-D08 处理导致成肌细胞增殖和分化失调。然而，需要进一步研究来调查 2-D08 对骨骼肌的长期影响。