Metabolic vulnerability of cancer stem cells and their niche.

Cancer stem cells (CSC) are the leading cause of the failure of anti-tumor treatments. These aggressive cancer cells are preserved and sustained by adjacent cells forming a specialized microenvironment, termed niche, among which tumor-associated macrophages (TAMs) are critical players. The cycle of tricarboxylic acids, fatty acid oxidation path, and electron transport chain have been proven to play central roles in the development and maintenance of CSCs and TAMs.

Basal nitric oxide release attenuates cell migration of HeLa and endothelial cells.

Nitric oxide (NO) generated by endothelial NO synthase (eNOS) is a key regulator of endothelial cell (EC) migration. Whereas the effects of acute NO generation are generally stimulatory, the role of chronic basal NO release has not been explored so far. Here, we addressed this question both in HeLa and in human endothelial cells.

Endothelial nitric oxide synthase is segregated from caveolin-1 and localizes to the leading edge of migrating cells.

The enzyme endothelial Nitric Oxide Synthase (eNOS) is involved in key physiological and pathological processes, including cell motility and apoptosis. It is widely believed that at the cell surface eNOS is localized in caveolae, where caveolin-1 negatively regulates its activity, however, there are still uncertainties on its intracellular distribution. Here, we applied high resolution confocal microscopy to investigate the surface distribution of eNOS in transfected HeLa cells and in human umbilical vein endothelial cells (HUVEC) endogenously expressing the enzyme.

A cellular system to study the role of nitric oxide in cell death, survival, and migration.

The gaseous messenger nitric oxide (NO) plays a bewildering number of roles in fundamental processes, such as cell locomotion, differentiation, proliferation and death. Its different and often contrasting roles may depend on its concentration and intracellular site of generation. We describe here a simple system with which to investigate the roles of NO generated at physiological levels in HeLa cells by eNOS transfected under an inducible promoter.