Glioblastoma multiforme (GBM) is a highly malignant devastating
brain tumor in adults.
Benzyl isothiocyanate (BITC) is one of the
isothiocyanates that have been shown to induce human
cancer cell apoptosis and cell cycle arrest. Herein, the effect of BITC on cell viability and apoptotic cell death and the genetic levels of human brain
glioblastoma GBM 8401 cells in vitro were investigated. We found that BITC induced cell morphological changes, decreased cell viability and the induction of cell apoptosis in GBM 8401 cells was time-dependent.
cDNA microarray was used to examine the effects of BITC on GBM 8401 cells and we found that numerous genes associated with cell death and cell cycle regulation in GBM 8401 cells were altered after BITC treatment. The results show that expression of 317 genes was upregulated, and two genes were associated with DNA damage, the DNA-damage-inducible transcript 3 (DDIT3) was increased 3.66-fold and the growth arrest and DNA-damage-inducible α (GADD45A) was increased 2.34-fold. We also found that expression of 182 genes was downregulated and two genes were associated with receptor for cell responses to stimuli, the
EGF containing
fibulin-like
extracellular matrix protein 1 (EFEMP1) was inhibited 2.01-fold and the
TNF receptor-associated protein 1 (TRAP1) was inhibited 2.08-fold. BITC inhibited seven mitochondria ribosomal genes, the mitochondrial
ribosomal protein;
tumor protein D52 (MRPS28) was inhibited 2.06-fold, the mitochondria
ribosomal protein S2 (MRPS2) decreased 2.07-fold, the mitochondria
ribosomal protein L23 (MRPL23) decreased 2.08-fold, the mitochondria
ribosomal protein S2 (MRPS2) decreased 2.07-fold, the mitochondria
ribosomal protein S12 (MRPS12) decreased 2.08-fold, the mitochondria
ribosomal protein L12 (MRPL12) decreased 2.25-fold and the mitochondria
ribosomal protein S34 (MRPS34) was decreased 2.30-fold in GBM 8401 cells. These changes of gene expression can provide the effects of BITC on the genetic level and are potential
biomarkers for
glioblastoma therapy.