Nitric oxide (NO) exerts physiopathological effects based mainly on its concentration. Thus, it facilitates or inhibits cancer-promoting characteristics. This review discusses the role of NO and its network of partners in tumor progression and angiogenesis: prostaglandin E 2 (PGE-2) and its producing enzymes, cyclooxigenase 2 (COX-2) and microsomal PGE synthase 1 (mPGES-1), and epidermal growth factor receptor (EGFR) signaling. Understanding the molecular mechanisms and cross-talk modulating NO effects by PGE-2 and EGFR and vice versa allows us to develop better therapeutic strategies for cancer treatment.
Donnini, S., Bazzani, L., Ziche, M., Terzuoli, E. (2016). Nitric oxide and PGE-2 cross-talk in EGFR-driven epithelial tumor cells. CRITICAL REVIEWS IN ONCOGENESIS, 21(5-6), 325-331 [10.1615/CritRevOncog.2017021204].
Nitric oxide and PGE-2 cross-talk in EGFR-driven epithelial tumor cells
Donnini, Sandra;Bazzani, Lorenzo;Ziche, Marina;Terzuoli, Erika
2016-01-01
Abstract
Nitric oxide (NO) exerts physiopathological effects based mainly on its concentration. Thus, it facilitates or inhibits cancer-promoting characteristics. This review discusses the role of NO and its network of partners in tumor progression and angiogenesis: prostaglandin E 2 (PGE-2) and its producing enzymes, cyclooxigenase 2 (COX-2) and microsomal PGE synthase 1 (mPGES-1), and epidermal growth factor receptor (EGFR) signaling. Understanding the molecular mechanisms and cross-talk modulating NO effects by PGE-2 and EGFR and vice versa allows us to develop better therapeutic strategies for cancer treatment.
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https://hdl.handle.net/11365/1031776