Cellular and molecular mechanisms of photodynamic hypericin therapy for nasopharyngeal carcinoma cells.

Hypericin-mediated photodynamic therapy (HY-PDT) has become a potential treatment for tumors and nonmalignant disorders. Some studies reported that HY-PDT could lead to apoptosis in some carcinoma cells. However, the molecular mechanism of HY-PDT remains unknown. In this study, we evaluated the molecular mechanisms of hypericin associated with light-emitting diode irradiation on the poorly differentiated human nasopharyngeal carcinoma cell line CNE-2 in vitro. To comprehensively understand the effects of HY-PDT on CNE-2 cells, we detected cell viability, cell cycle, apoptosis, intracellular glutathione content, and intracellular caspase (caspase-9, caspase-3, and caspase-8) activity. Furthermore, we performed genome-wide expression analysis via microarrays at different time points in response to HY-PDT, and we found that differentially expressed genes were highly enriched in the pathways related to reactive oxygen species generation, mitochondrial activity, DNA replication and repair, cell cycle/proliferation, and apoptosis. These results were consistent with our cytology test results and demonstrated that caspase-dependent apoptosis occurred after HY-PDT. Taken together, both cellular and molecular data revealed that HY-PDT could inhibit the growth of CNE-2 cells and induce their apoptosis.