Fig. 7
CMTM7 knockdown-mediated autophagy suppression contributes to tumor cell proliferation. A Control and CMTM7-knockdown A549 cells were plated at a cell density of 1.5 × 105/mL in a 6-well plate, and 24 h after plating, the cells were treated with CQ (12.5 μM) or control reagent, and cultured for 2 days and counted using a blood counting chamber. Data are representative of three independent experiments, and expressed as means ± s.d. (**P < 0.01; ns, not significant). B Control and CMTM7-knockdown A549 cells were plated as described in (A), and treated with rapamycin (RAPA, 50 nM) or DMSO as a vehicle control, and cell number was counted after 2 days via using a blood counting chamber. Data are representative of three independent experiments, and expressed as means ± s.d. (**P < 0.01). C Cell cycle distribution was assayed by flow cytometry. Representative histograms (left) and the percentages of G0/G1, S and G2/M phase cells (right) were shown. D Apoptosis was measured by FITC-Annexin-V/PI staining and flow cytometry. Scatter plots are representative of three independent experiments