Ferrous glycinate regulates cell energy metabolism via suppression of hypoxia-induced factor in human A549 cells

5^th International Conference and Exhibition on Metabolomics

May 16-18, 2016 Osaka, Japan

Jhong-Huei Jheng

Taipei Medical University, Taiwan

Posters & Accepted Abstracts: Metabolomics

Abstract :

HIF-1�±is a transcription factor and play a crucial role in cancer metabolism, which are characterized with aerobic glycolysis and suppressing of mitochondrial energy metabolism (Warburg effect). In the present study, we demonstrated that incubation of A549 cells with ferrous glycinate decreased the protein levels of HIF-1�± under either nomoxia or hypoxia conditions, which was further reversed by pretreatment with proteosome inhibitor, or prolyl hydroxylase inhibitor. The reduction of HIF-1�± level was associated with decreased expression levels of glucose transporter, Glut-1, and glycolytic enzymes including hexokinase-2, and lactate dehydrogenase A. On the other hand, treatment with ferrous glycinate reactivated oxidative phosphorylation by decreasing the expression of pyruvate dehydrogenase kinase-1 and pyruvate dehydrogenase phosphorylation that subsequently increased mitochondrial membrane potential and ATP production, suggesting ferrous glycinate regulate energy metabolism in lung adenocarcinoma cells. These results indicate that ferrous glycinate may serve as a therapeutic adjuvant for related human lung cancers.

Biography :

Jhong-Huei Jheng is a graduate student at the School of Medical Laboratory Sciences and Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.

Email: m609103002@tmu.edu.tw