Crosstalk of mTOR/PKM2 and STAT3/c ‐Myc signaling pathways regulate the energy metabolism and acidic microenvironment of gastric cancer

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. AbstractCancer 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 biologi cal 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, an d 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...
Source: Journal of Cellular Biochemistry - Category: Biochemistry Authors: Tags: RESEARCH ARTICLE Source Type: research