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NF‐κB in Photodynamic Therapy: Discrepancies of a Master Regulator
Author(s) -
Matroule JeanYves,
Volanti Cedric,
Piette Jacques
Publication year - 2006
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1562/2006-03-30-ir-862
Subject(s) - transcription factor , regulator , cancer research , nf κb , photodynamic therapy , inflammation , chemokine , microbiology and biotechnology , biology , cell adhesion molecule , signal transduction , matrix metalloproteinase , apoptosis , cancer cell , cancer , immunology , chemistry , gene , genetics , organic chemistry
Tumor eradication by photodynamic therapy (PDT) results from the onset of distinct killing processes. In addition to the well‐known necrotic and apoptotic mechanisms, PDT initiates an inflammatory response that will indirectly contribute to tumor clearance. The NF‐κB transcription factor is a major regulator of inflammation modulating the expression of cyto‐kines, chemokines, and adhesion molecules in various cell types in response to a large number of stimuli. Besides, NF‐κB regulates the expression of antiapoptotic genes, cyclooxygenases (COXs) and metalloproteinases (MMPs) as well, thereby favoring tumor cell proliferation and dissemination. In the present review, we aim to summarize the current knowledge on NF‐κB status following photosensitization of cancer cells and endothelial cells. In order to unravel the NF‐κB impact in PDT tumorigenicity and recurrences, we will stress the discrepancies of this major transcription factor relative to the signaling cascades underlying its activation and the cellular effects triggered by its translocation into the nucleus and its binding to its target genes.