Nakamura K, Nakajima Y, Nakamura Y
J Natl Cancer Inst. 1986 Nov;77(5):1035-8.
The glucose consumption of cultured murine (C57BL/6N) peritoneal exudate macrophages is suppressed by pleural effusions, ascitic fluids, and sera from patients with advanced primary lung and gastric cancers. Analysis for the generation of 14C-labeled CO2 after [14C]glucose metabolism revealed the glycolysis pathway to be more susceptible to cancerous body fluids than was the hexose monophosphate shunt. Enzymatic analysis showed that the enzyme susceptible to the cancerous body fluids was D-fructose-6-phosphate 1-phosphotransferase (PFK), the rate-limiting key enzyme in the glycolysis pathway. Other enzymes participating in glycolysis were insensitive to the cancerous body fluids. Suppression of PFK may represent a new tumor marker.
晚期原发性肺癌和胃癌患者的胸腔积液、腹水及血清可抑制培养的小鼠(C57BL/6N)腹腔渗出巨噬细胞的葡萄糖消耗。对[14C]葡萄糖代谢后14C标记二氧化碳生成的分析表明,糖酵解途径比磷酸己糖旁路更容易受到癌性体液的影响。酶学分析表明,对癌性体液敏感的酶是D-果糖-6-磷酸1-磷酸转移酶(PFK),它是糖酵解途径中的限速关键酶。参与糖酵解的其他酶对癌性体液不敏感。PFK的抑制可能代表一种新的肿瘤标志物。