| Autor: |
Hao-Sheng Chung, Chih-Hsuan Wu, Earl Fu, Yao-Dung Hsieh, Chung-Ren Jan, Pei-Feng Liu, Wei-Zhe Liang, Chih-Wen Shu |
| Rok vydání: |
2015 |
| Předmět: |
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| Zdroj: |
Lasers in Surgery and Medicine. 47:756-764 |
| ISSN: |
0196-8092 |
| DOI: |
10.1002/lsm.22419 |
| Popis: |
Background and Objectives Low-power laser irradiation (LPLI) is known to regulate cell proliferation and migration in clinical use. Recent studies have shown that LPLI induces cell death in some certain types of cancer cell lines. However, the cytotoxic selectivity of LPLI for cancer cells is not fully understood. The aim of this study was to compare the cytotoxic effects of LPLI in both human oral cancer OC2 cells and normal human gingival fibroblast (HGF) cells. Materials and Methods LPLI at 810 nm with an energy density from 10 to 60 J/cm2 was used to irradiate human oral cancer OC2 cells and normal HGF cells. Results We found that LPLI significantly diminished cell viability of human oral cancer OC2 cells due to cell cycle arrest at the G1 phase and the induction of cell death but that it had no or little effects on cell cycle progression and death in normal HGF cells. Moreover, the production of reactive oxygen species (ROS) and the loss of mitochondrial membrane potential (MMP) were elevated in human oral cancer OC2 cells compared with the un-irradiated cells. In contrast, these effects remained unchanged in normal HGF cells after exposure to LPLI. LPLI also induced apoptosis in caspase-3 dependent manner in human oral cancer OC2 cells, a mode of action that could be mediated by ROS and mitochondrial damage. Conclusion Our findings imply LPLI might be a potential therapy for oral cancers. Lasers Surg. Med. 47:756–764, 2015. © 2015 Wiley Periodicals, Inc. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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