Caspase-dependent signaling underlies glioblastoma cell death in response to the fungal metabolite, fusarochromanone

Fungal metabolites continue to show promise as a viable class of anticancer agents. In the present study, we investigated the efficacy of the fungal metabolite, fusarochromanone (FC101), for its antitumor activities in glioblastomas, which have a median survival of less than two years and a poor cli...

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Published in:International journal of molecular medicine 2014-09, Vol.34 (3), p.880-885
Main Authors: MAHDAVIAN, ELAHE, MARSHALL, MONIQUE, MARTIN, PATRICK M, CAGLE, PATRICE, SALVATORE, BRIAN A, QUICK, QUINCY A
Format: Article
Language:English
Subjects:
Apoptosis
Brain cancer
Breast cancer
Cell adhesion & migration
Cell death
Cell growth
fusarochromanone
glioblastoma
Glioblastoma multiforme
Laboratories
Leukemia
Medical research
Medicine, Experimental
Metabolites
Motility
Oxidative stress
poly(ADP-ribose) polymerase
Prostate
Proteins
Reactive oxygen species
Studies
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Summary:Fungal metabolites continue to show promise as a viable class of anticancer agents. In the present study, we investigated the efficacy of the fungal metabolite, fusarochromanone (FC101), for its antitumor activities in glioblastomas, which have a median survival of less than two years and a poor clinical response to surgical resection, radiation therapy and chemotherapy. Using clinically applicable doses, we demonstrated that FC101 induced glioblastoma apoptotic cell death via caspase dependent signaling, as indicated by the cleavage of poly(ADP-ribose) polymerase, glioblastoma (PARP). FC101 also induced differential reactive oxygen species (ROS) levels in glioblastoma cells, contrasting a defined role of oxidative stress in apoptotic cell death observed with other fungal metabolites. Furthermore, the antitumorigenic effects of FC101 on tumor cell migration were assessed. Cell migration assays revealed that FC101 significantly reduced the migratory capacity of glioblastomas, which are incredibly invasive tumors. Taken together, the present study establishes FC101 as a candidate anticancer agent for the cooperative treatment of glioblastomas.
ISSN:1107-3756
1791-244X
DOI:10.3892/ijmm.2014.1842