BDNF-AS downregulated the expression of FBXW7 and promoted the growth of GC cells by inhibiting FBXW7.Representative images of migratory or invaded cells (magnification, ×200) were shown. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Data were shown as mean ± SEM (n = 3). (A): The variation of FBXW7 mRNA expression level was detected by qRT-PCR assay after BDNF-AS overexpression or knockdown in HGC-27 and MKN-45 cells. (B): The variation of FBXW7 protein expression level was detected by western blotting after BDNF-AS overexpression or knockdown in HGC-27 and MKN-45 cells. (C): The mRNA expression levels of BDNF-AS and FBXW7 were obvious negative association in GC patients using pearson correlation analysis (Rs=-0.5001, p<0.0001). (D-F): Cell proliferation, invasion and migration ability of GC cells (HGC-27) negative control or treatment with BDNF-AS (PO-BDNF-AS or PO-BDNF-AS+PO-FBXW7) were detected by the colony formation (D), transwell (E) and wound healing assay (F) (magnification, 200×). (G-I): Cell proliferation, invasion and migration ability of GC cells (MKN-45) negative control or treatment with BDNF-AS (LV-SH-BDNF-AS or Lv-SH-BDNF-AS+SH-FBXW7) were detected by the colony formation (G), transwell (H) and wound healing assay (I) (magnification, 200×). (J): The level of ROS was detected by flow cytometry after BDNF-AS overexpression or combined overexpression of BDNF-AS and FBXW7 in erastin-treated (5 μM) GC cells (HGC-27) for 24 hours. DMSO served as a negative control. (K): The level of ROS was detected by flow cytometry after BDNF-AS knocked down or combined knockdown of BDNF-AS and FBXW7 in erastin-treated (5 μM) GC cells (MKN-45) for 24 hours. DMSO served as a negative control.