Abstract
Introduction:
Nasopharyngeal carcinoma (NPC) is one of the prevalent cancers among the Asian population. Photodynamic therapy (PDT) is a novel treatment approach for NPC that eradicates its biological targets via the generation of reactive oxygen species (ROS) by the combined usage of photosensitizer (PS), molecular oxygen, and light. PDT treatment with high specificity results in an enhanced patient quality of life. Recently, researchers looking for the modulation of cellular calcium ion levels to enhance PDT efficacy. However, there is no information on how the calcium ions levels affect the PDT efficacy. In this study, the effect of Thapsigargin (TG)-induced increase in calcium ion level on NPC cells and on PDT efficacy was investigated using C666-1/NPC cells.
Method:
The C666-1/NPC cells were cultured in a 96-well plate. TG was used to induce the release of calcium ions in the cytosol. The photosensitizer FosPeg was activated by a laser light source with 3J/cm2 for PDT treatment. The cytotoxic effects of TG, PDT, or combined usage of TG and PDT on NPC cells were measured by MTT assay.
Results & Discussion:
Our findings revealed that TG could induce C666-1/NPC cell death, with cell cytotoxicity of 3.2% and 14.1% obtained after 24 hours of incubation of 0.5mM and 1mM of TG respectively. The use of TG could also enhance PDT efficacy, with an 8% higher cell cytotoxicity obtained with 0.5mM of TG and 0.05mg/mL FosPeg activated at 3 J/cm2 when compared with FosPeg mediated PDT alone. The TG enhanced PDT efficacy might be due to the promotion of in-situ oxygen generation, causing an increase in ROS production.
Conclusion:
This study evident that calcium ion inducer TG could enhance FosPeg- mediated PDT efficacy on C666-1/NPC cells, suggesting that TG could serve as an adjuvant for PDT treatment. More in-depth mechanistic studies are deserved to reveal the relationship between the intracellular concentration of calcium ions and PDT efficacy.
Nasopharyngeal carcinoma (NPC) is one of the prevalent cancers among the Asian population. Photodynamic therapy (PDT) is a novel treatment approach for NPC that eradicates its biological targets via the generation of reactive oxygen species (ROS) by the combined usage of photosensitizer (PS), molecular oxygen, and light. PDT treatment with high specificity results in an enhanced patient quality of life. Recently, researchers looking for the modulation of cellular calcium ion levels to enhance PDT efficacy. However, there is no information on how the calcium ions levels affect the PDT efficacy. In this study, the effect of Thapsigargin (TG)-induced increase in calcium ion level on NPC cells and on PDT efficacy was investigated using C666-1/NPC cells.
Method:
The C666-1/NPC cells were cultured in a 96-well plate. TG was used to induce the release of calcium ions in the cytosol. The photosensitizer FosPeg was activated by a laser light source with 3J/cm2 for PDT treatment. The cytotoxic effects of TG, PDT, or combined usage of TG and PDT on NPC cells were measured by MTT assay.
Results & Discussion:
Our findings revealed that TG could induce C666-1/NPC cell death, with cell cytotoxicity of 3.2% and 14.1% obtained after 24 hours of incubation of 0.5mM and 1mM of TG respectively. The use of TG could also enhance PDT efficacy, with an 8% higher cell cytotoxicity obtained with 0.5mM of TG and 0.05mg/mL FosPeg activated at 3 J/cm2 when compared with FosPeg mediated PDT alone. The TG enhanced PDT efficacy might be due to the promotion of in-situ oxygen generation, causing an increase in ROS production.
Conclusion:
This study evident that calcium ion inducer TG could enhance FosPeg- mediated PDT efficacy on C666-1/NPC cells, suggesting that TG could serve as an adjuvant for PDT treatment. More in-depth mechanistic studies are deserved to reveal the relationship between the intracellular concentration of calcium ions and PDT efficacy.
Original language | English |
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Pages (from-to) | S1455-1456 |
Number of pages | 2 |
Journal | Annals of Oncology |
Volume | 34 |
Issue number | S3 |
DOIs | |
Publication status | Published - 14 Nov 2023 |