Caveolin-1 attenuates hydrogen peroxide-induced oxidative damage to lung carcinoma cells.

BACKGROUND

Oxidative stress has been shown to play an important role in cancer progression. In lung cancer, increasing expression of caveolin-1 (Cav-1) has been found in both primary and metastatic carcinomas and may be critical in the regulation of the oxidative status of cancer cells.

MATERIALS AND METHODS

Using molecular and pharmacological manipulations, the role of Cav-1 in regulating cellular oxidative status in lung cancer cells was investigated. The level of Cav-1 was determined by western blot analysis and reactive oxygen species (ROS) were detected by specific fluorescence probes.

RESULTS

The treatment of lung cancer H460 cells with hydrogen peroxide (H(2)O(2)) significantly up-regulated ROS inside the cells and contributed to cell apoptosis. While cells stably transfected with Cav-1 overexpressing plasmids (H460/Cav-1) exhibited decreased ROS signal and attenuated cell death rate, shRNACav-1 transfected (H460/shCav-1) cells showed enhanced ROS signal and increased cell damage. The use of specific superoxide anion and the hydrogen peroxide detecting assays and hydroxyl radical inhibition assay indicated that the variable oxidative stress found in these cells was mainly due to the alteration of the cellular hydroxyl radical level.

CONCLUSION

A novel role of Cav-1 protein is the suppression of cellular oxidative stress induced by H(2)O(2).