fig3
![Isocucurbitacin B inhibits glioma growth through PI3K/AKT pathways and increases glioma sensitivity to TMZ by inhibiting hsa-mir-1286a](https://image.oaes.cc/f7feab68-5c6b-49da-a16d-a6f35b649abb/cdr7001.fig.3.jpg)
Figure 3. (A) Relationship between mRNA expression levels of AKT1 and clinicopathological features in patients with glioma. Significant differences in the expression of (WHO II, WHO III, and WHO IV) (****P < 0.0001 vs. control group). Significant differences among different states of IDH (wild type, mutant type) (****P < 0.0001 vs. control group). Significant differences among different age status (</≥ 42) (*P < 0.05 vs. control group); (B) Relationship between mRNA expression levels of MAPK1 and clinicopathological features in patients with glioma. Significant differences in the expression of (WHO II, WHO III, and WHO IV) (****P < 0.0001 vs. control group). Significant differences among different states of IDH (wild type, mutant type) (****P < 0.0001 vs. control group); Significant differences among different age status (</≥ 42) (****P < 0.0001 vs. control group); (C and D) The prognosis of the low AKT1 and MAPK1 expression groups was better than that of the high expression group (*P < 0.05, ****P < 0.0001 vs. control group). The disease-free survival of the low AKT1 and MAPK1 expression groups was better thanthat of the high expression group (*P < 0.05 vs. control group). AKT1: AKT serine/threonine kinase 1; IDH: isocitrate dehydrogenase; MAPK1: mitogen-activated protein kinase 1.