@article {Chen:2014:1107-3756:17,
title = "DMS triggers apoptosis associated with the inhibition of SPHK1/NF-B activation and increase in intracellular Ca2+ concentration in human cancer cells",
journal = "International Journal of Molecular Medicine",
parent_itemid = "infobike://sp/ijmm",
publishercode ="sp",
year = "2014",
volume = "33",
number = "1",
publication date ="2014-01-01T00:00:00",
pages = "17-24",
itemtype = "ARTICLE",
issn = "1107-3756",
eissn = "1791-244X",
url = "https://www.ingentaconnect.com/content/sp/ijmm/2014/00000033/00000001/art00003",
doi = "doi:10.3892/ijmm.2013.1541",
author = "Chen and Pan and Gao and Yang and Wang and Peppelenbosch and Kong",
abstract = "N,N-Dimethyl-D-erythro-sphingosine (DMS) is known to induce cell apoptosis by specifically inhibiting sphingosine kinase1 (SPHK1) and modulating the activity of cellular ceramide levels. The present study investigated the effects and the mechanism(s) of action of DMS in human
lung cancer cells. We found that DMS dose-dependently suppressed cell proliferation and induced cell apoptosis in the human lung cancer cell line, A549. Mechanistically, treatment with DMS suppressed the activation of SPHK1 and nuclear factor-B (NF-B) p65, but increased intracellular
[Ca2+]i in A549 cells. This study demonstrates that DMS triggers the apoptosis of human lung cancer cells through the modulation of SPHK1, NF-B and calcium signaling. These molecules may represent targets for anticancer drug design.",
}