HIF2α, Hepcidin and their crosstalk as tumour-promoting signalling

被引:4
|
作者
Formica, Vincenzo [1 ]
Riondino, Silvia [1 ]
Morelli, Cristina [1 ,2 ]
Guerriero, Simona [1 ]
D'Amore, Federica [1 ]
Di Grazia, Antonio [3 ]
Blanco, Giovanna Del Vecchio [3 ]
Sica, Giuseppe [4 ]
Arkenau, Hendrik-Tobias [5 ]
Monteleone, Giovanni [3 ]
Roselli, Mario [1 ]
机构
[1] Univ Roma Tor Vergata, Dept Syst Med, Med Oncol Unit, Viale Oxford 81, I-00133 Rome, Italy
[2] Univ Roma Tor Vergata, PhD Program Syst & Expt Med Cycle 35, Via Montpellier 1, I-00133 Rome, Italy
[3] Univ Roma Tor Vergata, Dept Syst Med, Gastroenterol Unit, I-00133 Rome, Italy
[4] Univ Roma Tor Vergata, Dept Surg, Rome, Italy
[5] Sarah Cannon Res Inst UK, Drug Dev Unit, London, England
关键词
RENAL-CELL CARCINOMA; HYPOXIA-INDUCIBLE FACTOR; PHASE-II TRIAL; IRON-METABOLISM; DOWN-REGULATION; BREAST-CANCER; ALPHA EXPRESSION; GENE-EXPRESSION; ANEMIA; HIF-2-ALPHA;
D O I
10.1038/s41416-023-02266-2
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Not all aspects of the disruption of iron homeostasis in cancer have been fully elucidated. Iron accumulation in cancer cells is frequent for many solid tumours, and this is often accompanied by the contemporary rise of two key iron regulators, HIF2 alpha and Hepcidin. This scenario is different from what happens under physiological conditions, where Hepcidin parallels systemic iron concentrations while HIF2 alpha levels are inversely associated to Hepcidin. The present review highlights the increasing body of evidence for the pro-tumoral effect of HIF2 alpha and Hepcidin, discusses the possible imbalance in HIF2 alpha, Hepcidin and iron homeostasis during cancer, and explores therapeutic options relying on these pathways as anticancer strategies.
引用
收藏
页码:222 / 236
页数:15
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