Kruppel-like factor 2 disturb non-small cell lung cancer energy metabolism by inhibited glutamine consumption.

Abstract

OBJECTIVES:

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.

METHODS:

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.

KEY FINDINGS:

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.

CONCLUSIONS:

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.

• Authors: Song Xiao, Yan Jin-Xiang, Tian Long, Lu Xiu-Rong, Gao Hong, Yan Jie-Cheng, Zhang Fei
• Journal: The Journal of pharmacy and pharmacology (J Pharm Pharmacol) Vol. 72 Issue 6 Pg. 843-851 (Jun 2020) ISSN: 2042-7158 [Electronic] England
• PMID: 32196690 (Publication Type: Journal Article)
• Copyright: © 2020 Royal Pharmaceutical Society.

Chemical References

• KLF2 protein, human
• Kruppel-Like Transcription Factors
• Glutamine

Topics

• A549 Cells
• Carcinoma, Non-Small-Cell Lung (genetics, metabolism)
• Cell Line, Tumor
• Cell Proliferation (drug effects)
• Glutamine (metabolism)
• Glycolysis (drug effects)
• Humans
• Kruppel-Like Transcription Factors (genetics)