Fig. 4
CARM1 promotes the proliferation of GC cells through regulation of autophagy. A CCK-8 assay revealed that downregulation of CARM1 significantly suppressed the growth rate in HGC27 cells. B CARM1-knockdown and control HGC27 cells were treated with rapamycin (50 nM, 24 h). Cell viability was determined by CCK-8 assay. C CCK-8 assay proved that upregulation of CARM1 considerably enhanced cell viability in BGC823 cells. D CARM1-overexpressing and control BGC823 cells were treated with HCQ (25 μM, 24 h). Cell viability was determined by CCK-8 assay. E and F BGC823 cells stably transfected with overexpression or control lentivirus were treated with HCQ (25 μM) 3 days after cells were seeded. Cells were cultured for 10–14 days until visible clones were formed. G and H, HGC27 cells were transfected with CARM1 siRNA every 5 days to maintain the knockdown effect. Cells were cultured in medium containing rapamycin (50 nM) for 10–14 days until visible clones were formed. Representative images of clones are shown from three independent experiments. I Photographs of dissected xenograft tumors showed that the overexpression of CARM1 (top) promoted tumor growth in vivo compared to controls (bottom). J Tumor volumes at the indicated time points were evaluated by the formula: tumor volume (mm3) = [length (mm) × width (mm)2] × π/6. K Tumor weights indicated that the xenograft tumors derived from CARM1-overexpressing cells grew faster than those injected with control gastric cancer cells. Data are presented as the mean ± SD. *Represents *P < 0.05, **P < 0.01 and ***P < 0.001