Cell Death Pathways in Photodynamic Therapy of Cancer

Photodynamic therapy (PDT) is an emerging cancer therapy that uses the combination of non-toxic dyes or photosensitizers (PS) and harmless visible light to produce reactive oxygen species and destroy tumors. The PS can be localized in various organelles such as mitochondria, lysosomes, endoplasmic r...

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Main Authors:	Mroz, Pawel, Yaroslavsky, Anastasia, Kharkwal, Gitika B, Hamblin, Michael R.
Format:	Online
Language:	English
Published:	Molecular Diversity Preservation International (MDPI) 2011
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3729395/

id	pubmed-3729395
recordtype	oai_dc
spelling	pubmed-37293952013-07-31 Cell Death Pathways in Photodynamic Therapy of Cancer Mroz, Pawel Yaroslavsky, Anastasia Kharkwal, Gitika B Hamblin, Michael R. Review Photodynamic therapy (PDT) is an emerging cancer therapy that uses the combination of non-toxic dyes or photosensitizers (PS) and harmless visible light to produce reactive oxygen species and destroy tumors. The PS can be localized in various organelles such as mitochondria, lysosomes, endoplasmic reticulum, Golgi apparatus and plasma membranes and this sub-cellular location governs much of the signaling that occurs after PDT. There is an acute stress response that leads to changes in calcium and lipid metabolism and causes the production of cytokines and stress response mediators. Enzymes (particularly protein kinases) are activated and transcription factors are expressed. Many of the cellular responses center on mitochondria and frequently lead to induction of apoptosis by the mitochondrial pathway involving caspase activation and release of cytochrome c. Certain specific proteins (such as Bcl-2) are damaged by PDT-induced oxidation thereby increasing apoptosis, and a build-up of oxidized proteins leads to an ER-stress response that may be increased by proteasome inhibition. Autophagy plays a role in either inhibiting or enhancing cell death after PDT. Molecular Diversity Preservation International (MDPI) 2011-06-03 /pmc/articles/PMC3729395/ /pubmed/23914299 http://dx.doi.org/10.3390/cancers3022516 Text en © 2011 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Mroz, Pawel Yaroslavsky, Anastasia Kharkwal, Gitika B Hamblin, Michael R.
spellingShingle	Mroz, Pawel Yaroslavsky, Anastasia Kharkwal, Gitika B Hamblin, Michael R. Cell Death Pathways in Photodynamic Therapy of Cancer
author_facet	Mroz, Pawel Yaroslavsky, Anastasia Kharkwal, Gitika B Hamblin, Michael R.
author_sort	Mroz, Pawel
title	Cell Death Pathways in Photodynamic Therapy of Cancer
title_short	Cell Death Pathways in Photodynamic Therapy of Cancer
title_full	Cell Death Pathways in Photodynamic Therapy of Cancer
title_fullStr	Cell Death Pathways in Photodynamic Therapy of Cancer
title_full_unstemmed	Cell Death Pathways in Photodynamic Therapy of Cancer
title_sort	cell death pathways in photodynamic therapy of cancer
description	Photodynamic therapy (PDT) is an emerging cancer therapy that uses the combination of non-toxic dyes or photosensitizers (PS) and harmless visible light to produce reactive oxygen species and destroy tumors. The PS can be localized in various organelles such as mitochondria, lysosomes, endoplasmic reticulum, Golgi apparatus and plasma membranes and this sub-cellular location governs much of the signaling that occurs after PDT. There is an acute stress response that leads to changes in calcium and lipid metabolism and causes the production of cytokines and stress response mediators. Enzymes (particularly protein kinases) are activated and transcription factors are expressed. Many of the cellular responses center on mitochondria and frequently lead to induction of apoptosis by the mitochondrial pathway involving caspase activation and release of cytochrome c. Certain specific proteins (such as Bcl-2) are damaged by PDT-induced oxidation thereby increasing apoptosis, and a build-up of oxidized proteins leads to an ER-stress response that may be increased by proteasome inhibition. Autophagy plays a role in either inhibiting or enhancing cell death after PDT.
publisher	Molecular Diversity Preservation International (MDPI)
publishDate	2011
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3729395/
_version_	1611999533516980224

Cell Death Pathways in Photodynamic Therapy of Cancer

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