Fig. 6

CARM1 inhibitor rescued the tumor-promoting role of CARM1 both in vitro and in vivo. A Control and CARM1-overexpressing BGC823 cells were treated with CARM1i (8 μM, 24 h), and cell viability was determined by CCK-8 assay. B Control and CARM1-overexpressing BGC823 cells were cultivated in medium containing 8 μM CARM1i for 10–14 days. CARM1i reduced the increase in colony numbers caused by CARM1 overexpression. C and D Control and CARM1-overexpressing BGC823 cells were treated with CARM1i (8 μM, 24 h). Cell cycle phase distribution and apoptosis in the indicated cells were assessed by flow cytometry. E, F and G BGC823 xenograft models were generated to investigate the therapeutic effect of CARM1i and HCQ on GC in vivo. Nude mice injected with CARM1-overexpressing cells were randomly divided into four groups on day 6 when tumor volumes reached 50 mm³. CARM1i injection was performed twice daily at 100 mg/kg i.p. HCQ was administered once daily at 50 mg/kg i.p. The combination group was given two treatments, and the control group was intraperitoneally injected with PBS only. E Photograph of subcutaneous tumors dissected from animals in the indicated groups. F The tumor volumes were measured every four days and calculated by the formula: tumor volume (mm³) = [length (mm) × width (mm)²] × π/6. G The tumor weights were evaluated. Both CARM1i and HCQ slowed the tumor growth of GC. Furthermore, CARM1i exhibited a synergistic effect in combination with HCQ. Data are demonstrated as the mean ± SD. *Represents *P < 0.05, **P < 0.01 and ***P < 0.001