With its growth characteristic and chemoresistance,
glioblastoma is the most deadly
brain tumor. Twenty-five core genes that influence the chemosensitivity of
glioblastoma were screened in our previous experiments, and Id2, the inhibitor of
DNA binding 2, an oncogene encoding a helix-loop-helix
protein, was identified. The elevated expression levels of Id2 have been reported in several
malignancies. The aim of this study is to investigate the effects of Id2 expression on the chemosensitivity of
glioma cells. In this study, Id2 expression was investigated in a
malignant glioma cell line. Then, we silenced the expression of Id2 with the highly specific posttranscriptional suppression of RNA interference (RNAi) in U87 cells. The changes in response to
antitumor agents Me-CCNU,
VM26, and TMZ were evaluated by
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Apoptosis was measured using an
annexin V-
fluorescein isothiocyanate (
FITC) apoptosis detection kit. The relationship between Id2 expression and
caspase 3 was tested by RT-PCR and Western blot. This study demonstrated that Id2 was significantly upregulated in
glioma tissues, and Id2 correlated well with the advancement of
glioma grade and a worse prognosis in response to
temozolomide treatment. The RNAi-mediated decrease of Id2 expression enhanced chemosensitivity to
Me-CCNU,
VM26, and TMZ in the U87 cell line. We further discovered that silencing of Id2 expression could promote apoptosis of
glioblastoma cells, which could be attributed to the fact that Id2 affects
tumor cell chemosensitivity. Downregulation of the Id2 gene by RNAi could increase the chemosensitivity of
glioblastoma cells. Id2 could be a good molecular target for
glioblastoma gene therapy.