Glioblastoma is the most common primary malignant
tumor of the central nervous system, with an annual incidence of 5.26 per 100000 people. The clinical outcome of standard
therapy and the survival rate remain poor; therefore, there is an unmet need for a new strategy to treat this lethal disease. Although
amentoflavone was known to have anticancer potential in various types of
cancers, its antiglioblastoma ability and mechanism remain unrecognized. We demonstrated that
amentoflavone may suppress
glioblastoma invasion and migration by transwell assay. Moreover, we established NF- κ B reporter gene system and used that for verifying NF- κ B inhibition efficacy of
amentoflavone on in vitro and in vivo studies. Here, we indicated that
amentoflavone not only diminished NF- κ B activation, but also reduced NF- κ B-mediated downstream oncogenes expression, such as MMP-2, MMP-9, XIAP, cyclinD1 and
VEGF, which was elucidated by Western blot and immunohistochemistry (IHC).
Tumor growth inhibition and NF- κ B reduction was found in the
amentoflavone treatment group, which was revealed by the
glioblastoma-bearing animal model. In this study, we also used ERK inhibitor and NF- κ B inhibitor (QNZ) to confirm whether the beneficial result of
amentoflavone on
glioblastoma was mainly regulated by blockage of ERK/NF- κ B signaling. In summary, ERK/NF- κ B signaling pathway has a role in the inhibition of
tumor growth by
amentoflavone in
glioblastoma.