Journal
CANCER RESEARCH
Volume 67, Issue 1, Pages 149-159Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-06-2971
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Funding
- NATIONAL CANCER INSTITUTE [P01CA093900] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DENTAL &CRANIOFACIAL RESEARCH [R01DE013701] Funding Source: NIH RePORTER
- NCI NIH HHS [CA 93900] Funding Source: Medline
- NIDCR NIH HHS [DE 13701] Funding Source: Medline
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The generation of an 'angiogenic switch' is essential for tumor growth, yet its regulation is poorly understood. In this investigation, we explored the linkage between metastasis and angiogenesis through CXCL12/CXCR4 signaling. We found that CXCR4 regulates the expression and secretion of the glycolytic enzyme phosphoglycerate kinase 1 (PGK1). Overexpression of PGK1 reduced the secretion of vascular endothelial growth factor and interleukin-8 and increased the generation of angiostatin. At metastatic sites, however, high levels of CXCL12 signaling through CXCR4 reduced PGK1 expression, releasing the angiogenic response for metastastic growth. These data suggest that PGK1 is a critical downstream target of the chemokine axis and an important regulator of an 'angiogenic switch' that is essential for tumor and metastatic growth.
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