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Photobiomodulation Enhances Cisplatin Cytotoxicity in a Culture Model with Oral Cell Lineages
Authors:Ivana M. A. Diniz  Giovanna R. Souto  Iuri D. P. Freitas  José Alcides A. de Arruda  Janine M. da Silva  Tarcília A. Silva  Ricardo A. Mesquita
Affiliation:1. Department of Restorative Dentistry, School of Dentistry, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil;2. Department of Dentistry, School of Dentistry, Pontifícia Universidade Católica, Belo Horizonte, MG, Brazil;3. Department of Dentistry, School of Dentistry, Faculdade de SeteLagoas, SeteLagoas, MG, Brazil;4. Department of Oral Surgery and Pathology, School of Dentistry, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil
Abstract:Cisplatin plays a central role in cancer chemotherapy, but resistance to this drug remains a major obstacle in treatment. Drawbacks related to cisplatin failure may be associated with cell energy metabolism. This study investigated whether photobiomodulation (PBM) can potentiate the effects of cisplatin on keratinocytes (HaCat) and cancer cells (SCC25 and HN12). Cells were treated with laser (GaAlAs; 660 nm; 60 mW; 0.33 J; 2.14 W cm−2; 11.7 J cm−2 and 6 s) and cisplatin (7.8 μg mL−1) to evaluate cell viability, Ki-67, VEGF, TGF-β1, EGF expression and ROS production. Observations were validated in the SCC25 cell lineage, where the type of cell death (necrosis/apoptosis) and the amount of ATP were assessed. Cell lineages showed increased sensitivity to cisplatin associated with PBM (Cis-PBM). Ki-67 was augmented in all cell lineages treated with Cis-PBM when compared to cisplatin alone (Cis). Cis or Cis-PBM significantly decreased VEGF expression in cancer cells, while no changes were seen in the expression of TGF-β1 or EGF compared to control. ROS levels were similar in the Cis and Cis-PBM groups. Cells treated with Cis-PBM died by apoptosis, leading to greater consumption of ATP. These observations suggest that PBM may potentiate the effects of cisplatin, leading to increased drug cytotoxicity and enhanced cell death.
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