Mapping of oxidative stress responses of human tumor cells following photodynamic therapy using hexaminolevulinate

BMC Genomics. 2007 Aug 13:8:273. doi: 10.1186/1471-2164-8-273.

Abstract

Background: Photodynamic therapy (PDT) involves systemic or topical administration of a lesion-localizing photosensitizer or its precursor, followed by irradiation of visible light to cause singlet oxygen-induced damage to the affected tissue. A number of mechanisms seem to be involved in the protective responses to PDT, including activation of transcription factors, heat shock proteins, antioxidant enzymes and apoptotic pathways.

Results: In this study, we address the effects of a destructive/lethal hexaminolevulinate (HAL) mediated PDT dose on the transcriptome by using transcriptional exon evidence oligo microarrays. Here, we confirm deviations in the steady state expression levels of previously identified early defence response genes and extend this to include unreported PDT inducible gene groups, most notably the metallothioneins and histones. HAL-PDT mediated stress also altered expression of genes encoded by mitochondrial DNA (mtDNA). Further, we report PDT stress induced alternative splicing. Specifically, the ATF3 alternative isoform (deltaZip2) was up-regulated, while the full-length variant was not changed by the treatment. Results were independently verified by two different technological microarray platforms. Good microarray, RT-PCR and Western immunoblotting correlation for selected genes support these findings.

Conclusion: Here, we report new insights into how destructive/lethal PDT alters the transcriptome not only at the transcriptional level but also at post-transcriptional level via alternative splicing.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Activating Transcription Factor 3 / metabolism
  • Alternative Splicing / drug effects
  • Aminolevulinic Acid / analogs & derivatives*
  • Aminolevulinic Acid / pharmacology
  • Cell Line, Tumor
  • Cell Survival / drug effects
  • DNA, Mitochondrial / genetics
  • Dose-Response Relationship, Drug
  • Exons
  • Gene Expression Regulation / drug effects
  • Histones / genetics
  • Histones / metabolism
  • Humans
  • Jurkat Cells
  • Leukemia, T-Cell / drug therapy*
  • Leukemia, T-Cell / metabolism
  • Leukemia, T-Cell / pathology
  • MAP Kinase Kinase 4 / genetics
  • MAP Kinase Kinase 4 / metabolism
  • Metalloproteases / genetics
  • Metalloproteases / metabolism
  • Models, Biological
  • Oligonucleotide Array Sequence Analysis
  • Oxidative Stress / drug effects*
  • Photochemotherapy*
  • Photosensitizing Agents / pharmacology*
  • Protein Isoforms / genetics
  • Protein Isoforms / metabolism
  • Proto-Oncogene Proteins c-myc / genetics
  • Proto-Oncogene Proteins c-myc / metabolism
  • Time Factors
  • Transcription, Genetic / drug effects

Substances

  • ATF3 protein, human
  • Activating Transcription Factor 3
  • DNA, Mitochondrial
  • Histones
  • Photosensitizing Agents
  • Protein Isoforms
  • Proto-Oncogene Proteins c-myc
  • Aminolevulinic Acid
  • MAP Kinase Kinase 4
  • Metalloproteases
  • 5-aminolevulinic acid hexyl ester