Radiotherapy Department, The First Affiliated Hospital of Hebei North University, Zhangjiakou, China.
Neurosurgery Department, Ningyang No.1 People's Hospital, Ningyang, China.
J Pharm Pharmacol. 2020 Jun;72(6):843-851. doi: 10.1111/jphp.13252. Epub 2020 Mar 20.
Metabolic reprogramming is well accepted as a hallmark of cancer. This study aimed to explore the role of Kruppel-like factor 2 (KLF2) in aerobic glycolysis and glutamine consumption of energy metabolism in non-small cell lung cancer (NSCLC) cells.
Two different NSCLC cells, A549 and NCI-H1299, were used to investigate the role of KLF2 in glycolysis and glutamine consumption by tracer technique and KLF2 transfection.
The results showed that overexpression KLF could inhibit the energy metabolism and proliferation of NSCLC cells, but had no significant effect on glycolysis reaction and only affected the glutamine consumption of NSCLC cells. In NSCLC cells exposed to glutamine deprivation, the effect of overexpression of KLF2 on cell proliferation and energy metabolism disappeared. It was found that KLF2 could inhibit the expression of glutaminase (GLS) by metabolite tracing technique and so on. However, when GLS inhibitors were given to overexpressing KLF2 NSCLC cells, the intervention effect of KLF2 disappeared.
Kruppel-like factor 2 could decrease the level of glutamine, participate in the consumption of glutamine by cancer cells, and then inhibit the energy metabolism of cancer cells.
代谢重编程被广泛认为是癌症的一个标志。本研究旨在探讨 Kruppel 样因子 2（KLF2）在非小细胞肺癌（NSCLC）细胞有氧糖酵解和谷氨酰胺消耗能量代谢中的作用。
使用两种不同的 NSCLC 细胞系 A549 和 NCI-H1299，通过示踪技术和 KLF2 转染来研究 KLF2 在糖酵解和谷氨酰胺消耗中的作用。
结果表明，过表达 KLF 可以抑制 NSCLC 细胞的能量代谢和增殖，但对糖酵解反应没有显著影响，仅影响 NSCLC 细胞的谷氨酰胺消耗。在暴露于谷氨酰胺剥夺的 NSCLC 细胞中，过表达 KLF2 对细胞增殖和能量代谢的影响消失。研究发现，KLF2 可以通过代谢物示踪技术等抑制谷氨酰胺酶（GLS）的表达。然而，当给予过表达 KLF2 的 NSCLC 细胞 GL S 抑制剂时，KLF2 的干预作用消失。
Kruppel 样因子 2 可以降低谷氨酰胺水平，参与癌细胞对谷氨酰胺的消耗，从而抑制癌细胞的能量代谢。
