Fig. 6

miR-590-5p functions as a tumor suppressor in GC. a Ectopic transfection of miR-590-5p significantly suppressed proliferation in GC cell lines (**, P < 0.001). The mean and SDs obtained from six wells were plotted. b miR-590-5p transfection significantly inhibited anchorage-dependent colony formation ability (**, P < 0.001). Experiments were performed in triplicate. Error bars represent SDs. c Cell invasion ability was suppressed by miR-590-5p significantly (*, P < 0.05; **, P < 0.001). SDs were achieved from visions randomly selected. d Cell cycle distribution was examined by flow cytometry, which suggested G1 phase arrest in miR-590-5p-transfected cells. Experiments were conducted in triplicate. Statistical analysis of cell cycle percentages were presented by histograms (*, P < 0.05; **, P < 0.001). e Western blot analysis demonstrated the increased level of p21, p27, and reduction of pRb. Key factors in ATM signaling were activated in the miR-590-5p transfectants. f Immunofluorescence showed that γH2AX was significantly increased in GC cells with ectopic miR-590-5p expression. g Drug sensitivity was enhanced by miR-590-5p (*, P < 0.05). The cell viability was detected with different concentrations of Cisplatin. The mean and SDs were obtained from six wells. The largest mean was defined as 100% and the smallest mean defined as 0%. IC₅₀ values were calculated and listed in tables. h The expression correlation of miR-590-5p and related EMT markers in TCGA dataset. i The xenograft formation ability with stable miR-590-5p abundance was significantly inhibited compared with the negative control (*, P < 0.05). Black circles indicate the negative controls and red circles show the xenografts derived from miR-590-5p-transfected cells