p53 is an anti-cancer protein for inducing cell cycle arrest and apoptosis. In glioblastoma multiform (GBM), p53 is able to induce apoptosis via inhibition of its negative regulator Mdm2. Experimental studies have shown that microRNA-25 (miR-25) can repress Mdm2 expression and, in turn, stabilizes p53 to induce the G1/S checkpoint in GBM cells. miR-25 expression is regulated by the cell cycle inducer molecule E2F1, which has been reported to induce apoptosis when overexpressed in GBM. However, the way p53, E2F1, and miR-25 coordinately regulate apoptosis induction in GBM is still obscure in the literature. In this study, we propose a logical model contemplating the regulatory influence of miR-25 and its regulator E2F1 on cell fate decision. Through in silico results for the wild-type case, we observed that miR-25 may stabilize p53 expression through Mdm2 inhibition inducing a G1/S checkpoint arrest or apoptosis in cells overexpressing E2F1. The predicted probabilities of our mod...

中文翻译：

---

p53 / E2F1 / miR-25轴调节胶质母细胞瘤细胞的凋亡诱导：定性模型

p53是一种抗癌蛋白，可诱导细胞周期停滞和凋亡。在多形性胶质母细胞瘤（GBM）中，p53能够通过抑制其负调控因子Mdm2诱导凋亡。实验研究表明，microRNA-25（miR-25）可以抑制Mdm2表达，进而稳定p53以诱导GBM细胞中的G1 / S检查点。miR-25的表达受细胞周期诱导分子E2F1的调节，据报道该分子在GBM中过表达时会诱导细胞凋亡。然而，文献中仍然不清楚p53，E2F1和miR-25协同调节GBM中凋亡诱导的方式。在这项研究中，我们提出了一个逻辑模型，该模型考虑了miR-25及其调控因子E2F1对细胞命运决定的调控影响。通过针对野生型案例的计算机分析结果，我们观察到，miR-25可能通过抑制Mdm2来诱导过表达E2F1的细胞中G1 / S检查点停滞或凋亡而稳定p53的表达。我们模型的预测概率