Zohreh Azari - Department of Biochemistry, Faculty of Biological Science, Tarbiat Modares University, Tehran, Iran
Kayhan Mehdizadeh - Department of Biochemistry, Faculty of Biological Science, Tarbiat Modares University, Tehran, Iran
Farangis Ataei - Department of Biochemistry, Faculty of Biological Science, Tarbiat Modares University, Tehran, Iran
Saman Hosseinkhani - Department of Biochemistry, Faculty of Biological Science, Tarbiat Modares University, Tehran, Iran

Background: Glioblastoma is the most aggressive cerebral gliomas. Despite advances in therapies, the prognosis is still very poor. Therefore, novel therapeutic strategies are required. Inhibition of the proteasome ubiquitin pathway has shown to exert growth inhibitory effects on several human carcinoma cell lines. The inhibition of proteasome activity leads to cell death and also induces cell autophagy. Bortezomib is a reversible inhibitor of the 26S proteasome that shows potent antitumor activity in vitro and in vivo against several human cancers of adulthood. We therefore assessed whether bortezomib is capable of inducing apoptosis in U87 Glioblastoma cells. Material and methods: U87 cells were treated with increasing doses of bortezomib (0.1, 0.5, 1, 2, 4, 6, 10 nM) during a 72-hour period, and cell viability was measured by MTT assay and trypan blue and cell morphology.Results: U87 cells proliferation was inhibited in a dose-dependent manner. The mean bortezomib concentration that caused 50% inhibition (IC50) of growth was about 5 nM at 72 hours.Conclusion: Bortezomib sensitized U87 human cells to cell death and reduced its viability. These findings provide a basis for further investigations of bortezomib in the treatment of resistance cancer cell lines.

Bortezomib, Proteasome, U87, Survival, Apoptosis