S-Space College of Medicine/School of Medicine (의과대학/대학원) Program in Cancer Biology (협동과정-종양생물학전공) Journal Papers (저널논문_협동과정-종양생물학전공)
Hypoxia inhibits the SDF-1-dependent migration of human leukemic cell line HL-60 via blocking of Akt activation
- Seo, Young-Jin; Koh, Sang Hyeok; Kang, Hyoung Jin; Shin, Hee Young; Jeong, Gajin; Ahn, Hyo Seop
- Issue Date
- Biochem Biophys Res Commun. 2007 Dec 14;364(2):388-94. Epub 2007 Oct 15.
- Cell Hypoxia; Chemokine CXCL12/*metabolism; Chemotaxis; Chromones/pharmacology; Enzyme Inhibitors/pharmacology; Flavonoids/pharmacology; HL-60 Cells; Humans; Hypoxia-Inducible Factor 1, alpha Subunit/biosynthesis; Morpholines/pharmacology; Phosphorylation; Proto-Oncogene Proteins c-akt/antagonists & inhibitors/*metabolism; Receptors, CXCR4/biosynthesis
- Hypoxia is known to regulate the expression of genes involved in the migration of various cell types. Although many studies have shown that hypoxia increases cell migration, it still remains unclear whether hypoxia could modulate the stromal cell derived factor-1 (SDF-1)-dependent migration of leukemic cell. Herein, we demonstrated that the SDF-1-dependent migration of HL-60, was reduced under hypoxia with no comparable decrease of CXC-type chemokine receptor CXCR4, a cognate receptor for SDF-1. Furthermore, we showed that migration toward SDF-1 was reduced by inactivation of either serine/threonine kinase Akt or extracellular signal regulated kinase Erk, which was confirmed by selective pathway inhibitor LY294002 and PD98059. In our results, phosphorylation of Erk was increased under hypoxia, but phosphorylation of Akt was attenuated on the contrary. These results led us to conclusion that hypoxia could inhibit the SDF-1-dependent migration of HL-60 via blocking of Akt activation.
- 1090-2104 (Electronic)
- Files in This Item: There are no files associated with this item.