RETRACTED: A glycolytic mechanism regulating an angiogenic switch in prostate cancer (Retracted article. See vol. 81, pg. 1623, 2021)

被引:119
|
作者
Wang, Jianhua
Wang, Jincheng
Dai, Jinlu
Jung, Younghun
Wei, Chuen-Long
Wang, Yu
Havens, Aaron M.
Hogg, Phillip J.
Keller, Evan T.
Pienta, Kenneth J.
Nor, Jacques E.
Wang, Cun-Yu
Taichman, Russell S.
机构
[1] Univ Michigan, Sch Dent, Dept Periodont & Oral Med, Ann Arbor, MI 48109 USA
[2] Univ Michigan, Sch Dent, Dept Cariol Restorat Sci & Endodont, Ann Arbor, MI 48109 USA
[3] Univ Michigan, Sch Dent, Div Prosthodont, Dept Biol & Mat Sci, Ann Arbor, MI 48109 USA
[4] Univ Michigan, Sch Med, Dept Urol, Ann Arbor, MI 48109 USA
[5] Univ Michigan, Sch Med, Div Internal Med & Urol, Ann Arbor, MI 48109 USA
[6] Univ New S Wales, Ctr Vasc Res, Sydney, NSW, Australia
关键词
D O I
10.1158/0008-5472.CAN-06-2971
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:149 / 159
页数:11
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