fig2

Figure 2. PI3K-AKT signaling induces alkaliptosis resistance but does not affect cryptotanshinone sensitivity. (A) KEGG pathway analysis of DEGs based on mRNA transcriptomics; (B) Western blot analysis of indicated proteins in the indicated groups (Drug concentration: JTC801, 3.5 μM; treatment time: 24 h); (C) CCK-8 assay measuring cell viability after treatment with JTC801 or Crypto combined with MK-2206 (Drug concentrations: JTC801, 3.5 μM; MK-2206, 2 μM; treatment time: 24 h); (D) Cell death assay showing the proportion of dead cells following treatment with JTC801, MK-2206, or their combination (same concentrations and time as above). Data (C and D) are shown as mean ± SD from three or more biologically independent samples (C, n = 6; D, n = 3). Statistical significance was determined using two-way ANOVA with Tukey’s multiple comparisons test. Western blots (B) represent three independent experiments. Source data are provided. ^*P < 0.05 was considered statistically significant; ns: not significant. PI3K: Phosphatidylinositol-4,5-bisphosphate 3-kinase; AKT: AKT serine/threonine kinase; KEGG: Kyoto Encyclopedia of Genes and Genomes; DEGs: differentially expressed genes; SD: standard deviation; ANOVA: analysis of variance.