Synthesized Pheophorbide a-mediated photodynamic therapy induced apoptosis and autophagy in human oral squamous carcinoma cells
Article first published online: 28 JUN 2012
© 2012 John Wiley & Sons A/S
Journal of Oral Pathology & Medicine
Volume 42, Issue 1, pages 17–25, January 2013
How to Cite
Ahn, M. Y., Yoon, H.-E., Kwon, S.-M., Lee, J., Min, S.-K., Kim, Y.-C., Ahn, S.-G. and Yoon, J.-H. (2013), Synthesized Pheophorbide a-mediated photodynamic therapy induced apoptosis and autophagy in human oral squamous carcinoma cells. Journal of Oral Pathology & Medicine, 42: 17–25. doi: 10.1111/j.1600-0714.2012.01187.x
- Issue published online: 3 JAN 2013
- Article first published online: 28 JUN 2012
- Accepted for publication May 24, 2012
- oral sqaumous cell carcinoma;
- synthesized Pa-PDT
Background: Pheophorbide a (Pa) is a chlorine-based photosensitizer derived from an ethnopharmacological herb, and our group recently synthesized Pa by the removal of a magnesium ion and a phytyl group from chlorophyll-a. In this study, the effect of photodynamic therapy (PDT) with synthesized Pa was examined in a human oral squamous cell carcinoma (OSCC) cells.
Methods: Cells were treated with PDT with Pa, and reactive oxygen species (ROS) and mitochondrial membrane potential [ΔΨ (m)] were examined. Apoptosis was measured using annexin V staining and immunoblot. Autophagy was characterized by the increase in LC3B-II and the formation of autophagosome and acidic vesicular organelles (AVOs).
Results: Pa-PDT inhibited the proliferation of OSCC cells in a dose-dependent manner. Pa-PDT increased the number of apoptotic cells by inactivating ERK pathway. Pa-PDT also induced autophagy in OSCC cells evidenced by the increased levels of LC3 type II expression and the accumulation of AVOs. The inhibition of autophagy enhanced Pa-PDT-mediated cytotoxicity through an increase in necrosis.
Conclusions: These results suggest that synthesized Pa-PDT exerts anti-tumor effects by inducing apoptosis and autophagy and provide novel evidence that Pa-PDT induces autophagy, and autophagy inhibition enhances Pa-PDT-mediated necrosis in OSCC cells.