Journal
ONCOLOGY REPORTS
Volume 35, Issue 3, Pages 1557-1565Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/or.2015.4520
Keywords
CXCL16; autocrine; angiogenesis; hypoxia-inducible factor 1 alpha; Akt pathway; ERK pathway; p38 pathway
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Funding
- National Natural Science Funds [81102853, 81071841]
- Program for Excellent Scientific and Technological Innovation Team of Jiangsu Higher Education
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Chemokine (C-X-C motif) ligand 16 (CXCL16) is a new angiogenic factor inducing angiogenesis via extracellular signal-regulated kinases pathway. To further understand the molecular mechanism underlying CXCL16-induced angiogenesis, we explored involvement of other relevant pathways in CXCL16-induced angiogenesis. In the present study, we investigated the mechanisms underlying CXCL16-induced angiogenesis in human umbilical vein endothelial cells (HUVECs). CXCL16 promoted HUVEC proliferation, tube formation and migration. Enzyme-linked immunosorbent assay revealed that CXCL16 induced vascular endothelial growth factor secretion from HUVECs. Western blot analysis showed that CXCL16 increased the level of hypoxia-inducible factor 1 alpha, p-extracellular signal-regulated kinases (ERK), p-p38 and p-Akt dose-and time-dependently. ERK-, p38- and Akt-selective inhibitors significantly suppressed HUVEC proliferation, migration, tube formation and hypoxia-inducible factor 1a (HIF-1 alpha) expression induced by CXCL16. Furthermore, CXCL16 peptides induced CXCL16 secretion via ERK, p38 and Akt pathways, which was suppressed by HIF-1 alpha-selective inhibitor PX12. Our data suggest that CXCL16 induces angiogenesis in autocrine manner via ERK, Akt, p38 pathways and HIF-1 alpha modulation.
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