目的:酸性胃蛋白酶在喉癌中的致病机制尚不清楚。这项研究调查了酸性胃蛋白酶是否影响喉癌细胞中Glut-1的表达和糖酵解活性,以及它是否通过糖酵解在这些细胞的生长和迁移中起作用。
方法:体外研究。
方法:大学附属医院。
方法:用酸性胃蛋白酶和2-脱氧-d-葡萄糖(2-DG)处理喉癌TU212和TU686细胞,然后用Glut-1小干扰RNA(siRNA)转染。通过放射免疫分析计数器检测葡萄糖摄取,通过乳酸试剂盒检测乳酸分泌,通过蛋白质印迹检测Glut-1的表达。细胞活力,移民和入侵,和克隆形成使用细胞计数试剂盒-8,Transwell室,和克隆形成试验,分别。
结果:与对照组相比,酸性胃蛋白酶在喉癌细胞中的表达显着增加(P<0.01)。它还显着增强了18F-氟代脱氧葡萄糖(Cin/Cout)的摄取,乳酸分泌,细胞活力,迁移,入侵,喉癌细胞克隆形成与对照组比较(P<0.01)。糖酵解抑制剂2-DG和Glut-1siRNA可显著逆转酸性胃蛋白酶对喉癌细胞的作用(P<0.01)。
结论:酸性胃蛋白酶通过上调Glut-1促进喉癌细胞的生长和迁移,从而促进糖酵解。
OBJECTIVE: The 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.
METHODS: In vitro study.
METHODS: A university-affiliated hospital.
METHODS: Laryngeal 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.
RESULTS: Acidic 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).
CONCLUSIONS: Acidic
pepsin enhances the growth and migration of laryngeal carcinoma cells by upregulating Glut-1, thus promoting glycolysis.