Fingolimod (FTY720) reduces viability and survival and increases histone H3 acetylation in medulloblastoma cells.

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Perla AS, Fratini L, Cardoso PS, de Farias CB, da Cunha Jaeger M, Roesler R

Fingolimod (FTY720) reduces viability and survival and increases histone H3 acetylation in medulloblastoma cells.

Pediatr Hematol Oncol. 2020 Mar;37(2):170-175. doi: 10.1080/08880018.2019.1699213. Epub 2019 Dec 11.

PubMed ID

31826690 [ View in PubMed

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Abstract

Histone deacetylase inhibitors (HDACis) are epigenetic agents that display antitumor activities in experimental medulloblastoma (MB). Fingolimod (FTY720), an immunosuppressant agent currently used in the treatment of multiple sclerosis, also has anticancer actions and can act as an HDACi. Here we examined whether fingolimod can inhibit human MB cell viability and survival, and if the effects are accompanied by increased histone acetylation. D283 and DAOY MB cells were treated with different doses of fingolimod. Cell viability was assessed by cell counting in a hemocytometer, and cell survival was analyzed with a colony formation assay. Histone H3 acetylation was measured with an enzyme-linked immunosorbent assay (ELISA). Fingolimod at 7.5 or 10 muM, but not at 5 muM, induced a significant reduction in cell viability in D283 and DAOY cultures, and similar results were observed for inhibition of cell survival. In both cell lines, fingolimod also led to a significant increase in the levels of acetylated H3. These findings provide preliminary evidence indicating that fingolimod induces antitumor activities in MB, possibly through a mechanism which increases H3 histone acetylation.

DrugBank Data that Cites this Article

Drug Targets

Drug	Target	Kind	Organism	Pharmacological Action	Actions
Fingolimod	Histone deacetylase 1	Protein	Humans	Unknown	Inhibitor	Details