Background Gastric cancer is a very common type of tumor. Due to lack of molecular markers for early diagnosis, most gastric cancers are already in the intermediate-advanced state when they are diagnosed. Therefore, it is urgent to explore more effective prediction and treatment targets to improve the prognosis of patients with gastric cancer.
Objective To investigate the effect of long non-coding RNA CCAT2 (lncRNA CCAT2) on the glycolysis and proliferation of gastric cancer (GC) cells.
Methods siRNA (small interfering RNA) was used to knock down the expression of lncRNA CCAT2 in BGC-823 and HGC-27 cell lines. ATP, lactate acid, pyruvic acid production and glucose uptake were detected by colorimetry. The expression of glycolysis-related proteins was detected by Western blot. CCK-8 and EdU assays were used to detect the proliferation ability of GC cells.
Results siRNA was successfully transfected into BGC-823 and HGC-27 GC cells. The expression of lncRNA CCAT2 was downregulated. ATP (Adenosine Triphosphate), lactate acid, pyruvic acid production and glucose uptake were significantly suppressed (P＜0.05). The expression of GLUT1, HK2, PGAM1, and LDHɑ were significantly downregulated (P＜0.05). CCK-8 and EdU assays showed that the proliferation was inhibited after knocking down lncRNA CCAT2 (P＜0.05).
Conclusion lncRNA CCAT2 served as a regulator in the glucose metabolic reprogramming of GC cells. Knockdown of lncRNA CCAT2 can inhibit glycolysis and proliferation of GC cells.
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