Acidic Pepsin Affects Laryngeal Carcinoma Cell Growth and Invasion Through Glycolysis

Abstract

AbstractObjectiveThe pathogenic mechanism underlying the effects of acidic pepsin in laryngeal cancer remains unclear. This study investigated whether acidic pepsin influences Glut‐1 expression and glycolytic activity in laryngeal carcinoma cells and whether it plays a role in the growth and migration of these cells through glycolysis.Study DesignIn vitro study.SettingA university‐affiliated hospital.MethodsLaryngeal carcinoma TU 212 and TU 686 cells were treated with acidic pepsin and 2‐deoxy‐d‐glucose (2‐DG), then transfected with Glut‐1 small interfering RNA (siRNA). Glucose uptake was detected by a radioimmunoassay counter, lactate secretion was detected by a lactic acid kit, and Glut‐1 expression was detected by western blotting. Cell viability, migration and invasion, and clonal formation were assessed using the Cell Counting Kit‐8, Transwell chamber, and clonal formation assays, respectively.ResultsAcidic pepsin significantly increased Glut‐1 expression in laryngeal carcinoma cells compared with the control group (P < .01). It also significantly enhanced 18F‐fluorodeoxyglucose (Cin/Cout) uptake, lactate secretion, cell viability, migration, invasion, and clonal formation in laryngeal carcinoma cells compared with the control group (P < .01). The glycolytic inhibitor 2‐DG and Glut‐1 siRNA significantly reversed the effects of acidic pepsin on laryngeal carcinoma cells (P < .01).ConclusionAcidic pepsin enhances the growth and migration of laryngeal carcinoma cells by upregulating Glut‐1, thus promoting glycolysis.