Fig. 1

G-Rh2 inhibited tumor cell proliferation and promoted apoptosis in vitro. (A) Chemical structure of G-Rh2. (B, C) Viability of human A549 (B) and PC9 (C) cells assessed by CCK8 assays after 24-hours treatment with different concentrations of G-Rh2. (D, E) Effects of G-Rh2 on A549 (D) and PC9 (E) cell proliferation analyzed through CCK8 assays after IC50 treatment for 0, 24, 48, or 72 h. Data are expressed as mean ± SD. (F-I) EdU detection data showing A549 and PC9 cell proliferation ability following G-Rh2 treatment at 0, 30, or 40 µg/ml for A549 cells and 0, 30, or 35 µg/ml for PC9 cells for 24 h. Data are expressed as mean ± SD. (J-M) Colony formation assay, showing A549 and PC9 cell proliferation after G-Rh2 treatment at 0, 30, or 40 µg/ml for A549 cells and 0, 30, or 35 µg/ml for PC9 cells. Data are expressed as mean ± SD. (N-P) Flow cytometry measurement of the percentages of A549 and PC9 cells in G0/G1, S, and G2/M phases. Data are presented as the mean ± SD. (Q) Western blot detection of the cell cycle-associated protein Cyclin A2. (R-U) Flow cytometry analysis showing A549 and PC9 cell apoptosis after 24-hours treatment with 0, 30, 35, 40, or 45 µg/ml G-Rh2 Data are expressed as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.001 vs. the control group