Deactivation of cisplatin-resistant human lung/ovary cancer cells with pyropheophorbide-α methyl ester-photodynamic therapy
Autor: | Tinghe Yu, Guanhua Qian, Li Wang, Xueling Zheng |
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Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Cancer Research Programmed cell death Lung Neoplasms Porphyrins endocrine system diseases medicine.medical_treatment Apoptosis Photodynamic therapy Caspase 3 Biology 03 medical and health sciences 0302 clinical medicine medicine Humans Viability assay Cell Proliferation bcl-2-Associated X Protein Ovarian Neoplasms Pharmacology Cisplatin Errata Combined Modality Therapy Gene Expression Regulation Neoplastic 030104 developmental biology Photochemotherapy Proto-Oncogene Proteins c-bcl-2 Oncology A549 Cells Drug Resistance Neoplasm Cell culture 030220 oncology & carcinogenesis Immunology Cancer cell Cancer research Molecular Medicine Female Reactive Oxygen Species medicine.drug |
Zdroj: | Cancer Biology & Therapy. 18:984-989 |
ISSN: | 1555-8576 1538-4047 |
Popis: | The aim of this study was to determine whether photodynamic therapy (PDT) alone or combined with cisplatin (DDP), can deactivate cisplatin-resistant cancer cells. Human cancer cell lines A549 and SKOV3, and chemoresistant sublines A549/DDP and SKOV3/DDP, were subjected to PDT, DDP, or PDT combined with DDP. Cell viability and apoptosis were analyzed, and then intracellular reactive oxygen species (ROS) and proteins related to apoptosis were determined. PDT caused cell death, and PDT combined with DDP led to the highest percentage of dead cells in 4 cell lines; similar results were detected in ROS; a quantification evaluation manifested that the combined effect was addition. DDP increased the percentage of apoptotic cells, and the ROS level in A549 and SKOV3 cells, which was not observed in A549/DDP and SKOV3/DDP cells. Western blot revealed an increase of caspase 3 and Bax, and a decrease of Bcl-2, demonstrating the occurrence of apoptosis. The data suggest that PDT can efficiently deactivate resistant cells and enhance the action of DDP against resistant cancer cells. |
Databáze: | OpenAIRE |
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