Acridine orange is a molecule with fluorescence properties that was demonstrated to possess photosensitizing properties. The objective of this study was to investigate the photodynamic effect of acridine orange on glioblastoma cell viability and growth.
Glioblastoma cells (n = 8000 cells/well at 0 hours) were exposed to acridine orange followed by white unfiltered light-emitting diodes (LED) light. Cultures were exposed to either 10 or 30 minutes of light. The cell number per well was determined at 0, 24, 48, and 72 hours after exposure.
A dramatic cytocidal effect of acridine orange after exposure to as little as 10 minutes of white light was observed. There was almost complete eradication of the glioblastoma cells over a 72-hour period. Although acridine orange or light alone exhibited some effect on cell growth, it was not as pronounced as the combination of acridine orange and light.
This is the first study to demonstrate the photodynamic effect of acridine orange in glioblastoma cells. This data supports the need for further studies to characterize and evaluate whether this striking cytotoxic effect can be achieved in vivo. The combination of acridine orange and exposure to white unfiltered LED light may have potential future applications in management of glioblastoma 1).
In a study, Wang et al. determined if juglone exerts antitumor effects in the U251 human glioma cell line and investigated its potential underlying molecular mechanisms. Cell survival, apoptosis, migration, angiogenesis and molecular targets were identified with multiple detection techniques including the MTT cell proliferation assay, dual acridine orange/ethidium bromide staining, electron microscopy, transwell migration assay, chick chorioallantoic membrane assay, quantitative real-time polymerase chain reaction and immunoblotting. The results showed that 5-20 µM juglone markedly suppressed cell proliferation, induced apoptosis, and enhanced caspase-3 activity in U251 cells in a dose- and time-dependent manner. Moreover, juglone inhibited cell migration and the formation of new blood vessels. At the molecular level, juglone markedly suppressed Pin1 levels in a time-dependent manner. TGF-β1/Smad signaling, a critical upstream regulator of miR-21, was also suppressed by juglone. Moreover, the transient overexpression of Pin1 reversed its antitumor effects in U251 cells and inhibited juglone-mediated changes to the TGF-β1/miR-21 signaling pathway. These findings suggest that juglone inhibits cell growth by causing apoptosis, thereby inhibiting the migration of U251 glioma cells and disrupting angiogenesis; and that Pin1 is a critical target for juglone's antitumor activity. The present study provides evidence that juglone has in vitro efficacy against glioma. Therefore, additional studies are warranted to examine the clinical potential of juglone in human gliomas 2).