HENMT1通过激活PI3K-AKT-mTOR信号通路促进胃癌的增殖与迁移
HENMT1 promotes the proliferation and migration of gastric cancer by activating the PI3K-AKT-mTOR signaling pathway
Note： A. Western blotting was used to assess HENMT1's impact on key protein expression in the PI3K-AKT-mTOR pathway in GC cell line. B. The impact of si/over HENMT1 with 740 Y-P/3-MA on HGC27 and AGS GC cell survival was evaluated using the CCK-8 assay. C/D. The impact of si/over HENMT1 with 740 Y-P/3-MA on the migration of GC cell lines HGC27 and AGS was assessed through cell scratch (C) and Transwell assay (D). E/F. Western blotting was employed to assess protein changes linked to cell migration (E) and key components of the PI3K-AKT-mTOR pathway (F) in HGC27 and AGS GC cell lines following combined treatment with si/over HENMT1 and 740 Y-P/3MA.①P=0.010, ③P=0.002, ⑤P=0.045, compared with the siNC+DMSO group; ②P=0.005, ④P<0.001, ⑥P=0.028, compared with the siNC+740 Y-P group; ⑦P<0.001, ⑨P=0.033, ⑪P=0.030, compared with the Vector+DMSO group; ⑧P<0.001, ⑩P=0.030, ⑫P=0.003, compared with the Vector+3-MA group.
