Cancer cells consume large amounts of
glucose to produce
lactate, even in the presence of ample
oxygen. This phenomenon is called the Warburg effect. c-Myc is an important member of the Myc gene family and is involved in the development of various
tumors. It plays an important role in the regulation of
tumor energy metabolism, which can regulate glycolysis to promote the Warburg effect in a
tumor. Our study aimed to improve the malignant
biological behavior by controlling the energy metabolism of
gastric cancer through the mTOR/PKM2 and signal transduction and activator 3 (STAT3)/c-Myc signaling pathways through a series of in vitro experiments. Human
gastric cancer AGS and HGC-27 cells were treated with PKM2 and c-Myc lentivirus, and the effects of the knockdown of PKM2 and/or c-Myc were analyzed on cell proliferation, cell apoptosis, the ability of cell migration, and the growth signaling pathway in vitro. The expressions of PKM2, c-Myc, LDHA, STAT3, P-STAT3, GLUT-1 gene were identified by the quantitative real-time polymerase chain reaction and Western blot analysis.
Lactate and
glucose levels were tested by the corresponding kit. Our findings showed that PKM2 and c-Myc were upregulated in human
gastric cancer. Knockdown of c-Myc in
gastric cancer cells suppressed cell proliferation capacity and glycolysis level, and the inhibitory effects on
gastric cancer cells upon co-knockdown of PKM2 and c-Myc were more obvious compared with knockout of PKM2 or c-Myc alone. And there was a correlation between the mTOR/PKM2 and the STAT3/c-Myc signaling pathways. Our results suggested that c-Myc might be considered a potential therapeutic target for
gastric cancer and PKM2 combined with c-Myc could better inhibit the malignant
biological behaviors of
gastric cancer.