fig3

Isocucurbitacin B inhibits glioma growth through PI3K/AKT pathways and increases glioma sensitivity to TMZ by inhibiting hsa-mir-1286a

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.

Cancer Drug Resistance
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