Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Harada, K. et al.

Harada, Supriatno, Kawashima, Yoshida, Sato,

S-1 inhibits tumorigenicity and angiogenesis of human oral squamous cell carcinoma cells by suppressing expression of phosphorylated Akt, vascular endothelial growth factor and fibroblast growth factor-2.

It has been reported that S-1 can exert antitumor effects on various human cancers including oral squamous cell carcinoma (OSCC). However, little is known about the detailed mechanisms of the antitumor activity of S-1. In the present study, we determined whether S-1 could suppress the angiogenesis and growth of human OSCC cells in vitro and in vivo. The S-1 component (5-FU plus CDHP) significantly suppressed the growth and migration of OSCC cells and BAEC, which inhibited tubule formation in HUVECs in vitro. Also, S-1 inhibited the nuclear factor-kappaB (NF-kappaB) activity in human OSCC cells in vitro. Moreover, S-1 inhibited the expression of survival signal, phosphorylated Akt (p-Akt), and of two major proangiogenic molecules, vascular endothelial growth factor (VEGF) and fibroblast growth factor-2 ( FGF-2), in cells implanted into the subcutaneous tissue of nude mice. The decreased expression of p-Akt, VEGF and FGF-2 correlated with decreased tumorigenicity and decreased vascularization of lesions in vivo. These findings suggest that S-1 can suppress the angiogenesis and growth of OSCC cells by inhibiting the expression of p-Akt, VEGF and FGF-2 involved in the blockade of Akt/NF-kappaB pathway.[1]

References

S-1 inhibits tumorigenicity and angiogenesis of human oral squamous cell carcinoma cells by suppressing expression of phosphorylated Akt, vascular endothelial growth factor and fibroblast growth factor-2. Harada, K., Supriatno, n.u.l.l., Kawashima, Y., Yoshida, H., Sato, M. Int. J. Oncol. (2007) [Pubmed]

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