Effect of S1P5 on proliferation and migration of human esophageal cancer cells

Abstract

S1P binding to S1P5 inhibits the proliferation and migration of S1P5-transfected Eca109 cells. Esophageal cancer cells may down-regulate the expression of S1P5 to escape the inhibitory effect.

Transforming growth factor β2 (TGF-β2)-induced connective tissue growth factor (CTGF) expression requires sphingosine 1-phosphate receptor 5 (S1P5) in human mesangial cells

“…Moreover, S1P 5 plays an important role for the trafficking of natural killer cells [22,23]. In contrast, anti-migratory and anti-proliferative effects were shown upon activation of S1P 5 in human esophageal cancer cells [24] and oligodendrocytes [25].…”

Expression profile of the sphingosine kinase signalling system in the lung of patients with chronic obstructive pulmonary disease

“…S1PR5 has been previously reported to inhibit the proliferation and migration of epithelial cells of the oesophagus. Additionally, the growth of oesophageal cancer reduced the expression of S1PR5 mRNA (Hu et al, 2010). Therefore, the downregulation of this receptor may well contribute to the establishment of a 'pro-tumour environment' in COPD.…”

Extracellular and intracellular sphingosine-1-phosphate in cancer

“…In contrast to LGL, human Eca109 esophageal squamous carcinoma cells express significantly lower levels of S1PR5 than normal esophageal mucosal epithelium. In addition, overexpression of S1PR5 inhibited proliferation and migration of these cells, suggesting that downregulation of S1PR5 provides an inhibitory signal [138].…”