Deltonin enhances gastric carcinoma cell apoptosis and chemosensitivity to cisplatin via inhibiting PI3K/AKT/mTOR and MAPK signaling

Figure 1 Deltonin inhibits gastric carcinoma cell proliferation and expedites their apoptosis. A: Gastric carcinoma (GC) cell lines AGS, HGC-27, and MKN-45 were treated with deltonin (0 μM, 0.625 μM, 1.25 μM, 2.5 μM, 5 μM, 10 μM, and 20 μM) for 24 h. 3-(4,5-dimethylthiazol-2-yl)-3,5-diphenyltetrazolium bromide (MTT) assay was used to examine cell viability; B: IC₅₀ values of AGS, HGC-27, and MKN-45 cells treated with deltonin of different concentrations; C: Flow cytometry analysis of apoptosis of AGS, HGC-27, and MKN-45 cells treated with 2.5 μM deltonin for 24 h; D: Western blot analysis of expression of apoptosis-concerned proteins (Bax, Bak, Bid, and Fas) and DNA repair-associated proteins (Rad51 and MDM2) in GC cells; E: Western blot analysis of protein expression in AGS cells treated with 2.5 μM of deltonin for 0 h, 24 h, 48 h, and 72 h; F: Western blot analysis of protein expression in AGS cells treated with deltonin (0, 2.5, 5, and 10 μM) for 24 h; G: Western blot analysis of protein expression in HGC-27 cells treated with 2.5 μM of deltonin for 0 h, 24 h, 48 h, and 72 h; H: Western blot analysis of protein expression in HGC-27 cells treated with deltonin (0, 2.5, 5, and 10 μM) for 24 h; NS: P > 0.05, ^aP < 0.05, ^bP < 0.01, ^cP < 0.001 vs control group. n = 3. NS: No significance; PI3K: Phosphatidylinositol 3-kinase; AKT: Protein kinase B; mTOR: Mammalian target of the rapamycin; p38-MAPK: p38-mitogen-activated protein kinase.