Gene Expression Profile of Lung Cancer Cells Following Photodynamic Therapy.
- Author:
Ji Hyun SUNG
1
;
Mi Eun LEE
;
Seon Sook HAN
;
Seung Joon LEE
;
Kwon Soo HA
;
Woo Jin KIM
Author Information
- Publication Type:Original Article
- Keywords: Gene expression profiling; Lung neoplasms; Photosensitizing agents
- MeSH: Antigens, CD46; Carbonic Anhydrases; Cell Death; Cell Line; Cell Survival; Clusterin; Complement System Proteins; Flow Cytometry; Gene Expression Profiling; Gene Expression*; Lung Neoplasms*; Lung*; Membrane Proteins; Necrosis; Phosphoglycerate Dehydrogenase; Photochemotherapy*; Photosensitizing Agents; Ribosomal Proteins; Sequence Analysis, DNA; Transcriptome*
- From:Tuberculosis and Respiratory Diseases 2007;63(1):52-58
- CountryRepublic of Korea
- Language:Korean
- Abstract: BACKGROUND: Photodynamic therapy is a viable option for lung cancer treatment, and many studies have shown that it is capable of inducing cell death in lung cancer cells. However, the precise mechanism of this cell death has not been fully elucidated. To investigate the early changes in cancer cell transcription, we treated A549 cells with the photosensitizer DH-I-180-3 and then we illuminated the cells. METHODS: We investigated the gene expression profiles of the the A549 lung cancer cell line, using a DEG kit, following photodynamic therapy and we evaluated the cell viability by performing flow cytometry. We identified the genes that were significantly changed following photodynamic therapy by performing DNA sequencing. RESULTS: The FACS data showed that the cell death of the lung cancer cells was mainly caused by necrosis. We found nine genes that were significantly changed and we identified eight of these genes. We evaluated the expression of two genes, 3-phosphoglycerate dehydrogenase and ribosomal protein S29. The expressed level of carbonic anhydrase XII, clusterin, MRP3s1 protein, complement 3, membrane cofactor protein and integrin beta 1 were decreased. CONCLUSION: Many of the gene products are membrane-associated proteins. The main mechanism of photodynamic therapy with using the photosensitizing agent DH-I-180-3 appears to be necrosis and this may be associated with the altered production of membrane proteins.
