GBM 是最具威胁性的脑肿瘤。 GBM 的发展是由癌细胞的生长、浸润和运动推动的。了解潜在机制和识别新的治疗药物对于有效治疗 GBM 至关重要。我们的研究重点是检查 EnHydrin 对实验室环境和生物体内 GBM 细胞破坏活性的抑制影响。通过网络药理学和生物信息学分析，我们确定Jun为目的基因，EMT为关键信号通路。从机制上来说，Enhydrin 抑制靶基因 Jun 的活性，从而增加 Smad7 的表达，Smad7 受转录因子 Jun 无限调节，而作为抑制性转录因子，Smad7 可以下调 TGF-β1 以及随后的 Smad2/3 信号传导途径。因此，整个过程极大地阻碍了GBM的EMT机制，导致细胞增殖、侵袭和迁移显着下降。总之，我们的研究表明 EnHydrin 通过关注 Jun/Smad7/TGF-β1 信号通路来阻碍 EMT，为治疗 GBM 提供了一个有希望的靶点。此外，EnHydrin 作为治疗 GBM 的新药物展现出令人鼓舞的前景。版权所有 © 2024。由 Elsevier Inc. 出版。

GBM is the most threatening form of brain tumor. The advancement of GBM is propelled by the growth, infiltration, and movement of cancer cells. Understanding the underlying mechanisms and identifying new therapeutic agents are crucial for effective GBM treatment. Our research focused on examining the withhold influence of Enhydrin on the destructive activity of GBM cells, both in laboratory settings and within living organisms. By employing network pharmacology and bioinformatics analysis, we have determined that Jun serves as the gene of interest, and EMT as the critical signaling pathway. Mechanistically, Enhydrin inhibits the activity of the target gene Jun to increase the expression of Smad7, which is infinitively regulated by the transcription factor Jun, and as the inhibitory transcription factor, Smad7 can down-regulate TGF-β1 and the subsequent Smad2/3 signaling pathway. Consequently, this whole process greatly hinders the EMT mechanism of GBM, leading to the notable decline in cell proliferation, invasion, and migration. In summary, our research shows that Enhydrin hinders EMT by focusing on the Jun/Smad7/TGF-β1 signaling pathway, presenting a promising target for treating GBM. Moreover, Enhydrin demonstrates encouraging prospects as a new medication for GBM treatment.Copyright © 2024. Published by Elsevier Inc.