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MG132, a proteasome inhibitor decreased the growth of Calu-6 lung cancer cells via apoptosis and GSH depletion
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Abstract
The inhibition of proteasome function has emerged as a useful strategy to maneuver
apoptosis. In the present study, we evaluated the effects of MG132 as a proteasome
inhibitor on the growth of Calu-6 lung cancer cells in relation to the cell cycle,
cell death, reactive oxygen species (ROS) and glutathione (GSH) levels. MG132 dose-dependently
inhibited the growth of Calu-6 cells at 24h. DNA flow cytometric analysis indicated
that 1-30 microM MG132 induced an S phase arrest in Calu-6 cells. MG132 also induced
apoptosis, which was accompanied by the loss of mitochondrial membrane potential (MMP;
Deltapsi(m)). The pan-caspase inhibitor (Z-VAD) significantly rescued Calu-6 cells
from MG132-induced cell death. The intracellular ROS levels including O(2)(-) were
increased in MG132-treated Calu-6 cells. MG132 also increased GSH-depleted cell numbers
in Calu-6 cells. Z-VAD significantly decreased O(2)(-) levels and GSH-depleted cell
numbers in MG132-treated Calu-6 cells. In conclusion, MG132 inhibited the growth of
Calu-6 cells via apoptosis and GSH depletion.
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