Fig. 1: (S)-crizotinib inhibits gastric cancer cell growth.

Cultured SGC-7901 and BGC-823 cells were exposed to increasing concentrations of (S)-crizotinib for 24 h, and in vitro cell growth assays prepared for the analysis as described below. a Viability of gastric cancer cells in response to (S)-crizotinib was measured by the MTT assay; average absorbance ± SEM values are graphed against (S)-crizotinib concentrations; n = 4; IC₅₀ is indicated on lower left of graph. b Induction of apoptosis in response to (S)-crizotinib: was determined by annexin V/PI staining. DMSO was used as control; shown is representative flow cytometric analysis. c Quantification of apoptotic cells presented as percent total, average ± SEM; n = 4; (*p < 0.05, **p < 0.01 compared to DMSO). d Representative Western blot analysis of apoptosis-related, cle-PARP (Poly ADP-ribose polymerase) following exposure to (S)-crizotinib for 20 h; GAPDH was used as loading control; n = 4. e Induction of cell cycle arrest in gastric cancer cells was determined by PI staining following exposure to (S)-crizotinib for 14 h; shown is representative flow cytometric analysis. f Histograms showing cell cycle distributions from flow data collected from e; n = 4. g Representative Western blot analysis of key G2/M cell cycle-related proteins: murine double minute 2 (MDM-2), Cyclin B1, and cell division cycle protein 2 (Cdc2) in cells treated with (S)-crizotinib for 14 h; GAPDH as loading control; n = 4