LINC01123通过结合ENO1促进胃癌的增殖和糖酵解

张舒琼, 柯星, 赵兴贺, 陈晓翠, 郑浩东, 陈惠, 沈立松, 杨俊瑶

LINC01123 promotes proliferation and glycolysis of gastric cancer via binding to ENO1

ZHANG Shuqiong, KE Xing, ZHAO Xinghe, CHEN Xiaocui, ZHENG Haodong, CHEN Hui, SHEN Lisong, YANG Junyao

图7 LINC01123通过ENO1发挥的促增殖、迁移、侵袭和糖酵解功能 Note： A. ENO1 expression after transfection of ENO1 siRNA in LINC01123-overexpressing gastric cancer MKN-45 and HGC-27 cell lines. B. CCK-8 assay showing that the proliferation of MKN-45 and HGC-27 cells overexpressing LINC01123 decreased after ENO1 knockdown. C. Wound healing assay showing that the migration of MKN-45 and HGC-27 cells overexpressing LINC01123 decreased after ENO1 knockdown. D. Transwell migration assay showing that the migration of MKN-45 cells overexpressing LINC01123 decreased after interference with ENO1 expression. E. Transwell invasion assay showing that the invasion of MKN-45 cells overexpressing LINC01123 decreased after ENO1 knockdown. F/G. ENO1 knockdown reduces LINC01123-induced lactate production (F) and ATP production (G) in MKN-45 and HGC-27 cells overexpressing LINC01123. ①P<0.001, ②P=0.008, ③P=0.006, ④P=0.001, ⑤P=0.007, ⑥P=0.002, ⑦P=0.012, ⑧P=0.020, ⑨P=0.011, ⑩P=0.004.

Fig 7 Promotion of proliferation, migration, invasion, and glycolysis by LINC01123 via ENO1