Cell death pathways in photodynamic therapy of cancer

Pawel Mroz, Anastasia Yaroslavsky, Gitika B. Kharkwal, Michael R. Hamblin

Research output: Contribution to journalReview article

281 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)2516-2539
Number of pages24
JournalCancers
Volume3
Issue number2
DOIs
StatePublished - Jun 1 2011

Fingerprint

Photochemotherapy
Cell Death
Photosensitizing Agents
Neoplasms
Mitochondria
Apoptosis
Autophagy
Golgi Apparatus
Proteasome Endopeptidase Complex
Caspases
Cytochromes c
Lysosomes
Lipid Metabolism
Endoplasmic Reticulum
Organelles
Protein Kinases
Reactive Oxygen Species
Proteins
Transcription Factors
Coloring Agents

Keywords

  • Apoptosis
  • Autophagy
  • Cancer
  • Cell death
  • Necrosis
  • Photodynamic therapy

Cite this

Mroz, P., Yaroslavsky, A., Kharkwal, G. B., & Hamblin, M. R. (2011). Cell death pathways in photodynamic therapy of cancer. Cancers, 3(2), 2516-2539. https://doi.org/10.3390/cancers3022516

Cell death pathways in photodynamic therapy of cancer. / Mroz, Pawel; Yaroslavsky, Anastasia; Kharkwal, Gitika B.; Hamblin, Michael R.

In: Cancers, Vol. 3, No. 2, 01.06.2011, p. 2516-2539.

Research output: Contribution to journalReview article

Mroz, P, Yaroslavsky, A, Kharkwal, GB & Hamblin, MR 2011, 'Cell death pathways in photodynamic therapy of cancer', Cancers, vol. 3, no. 2, pp. 2516-2539. https://doi.org/10.3390/cancers3022516
Mroz P, Yaroslavsky A, Kharkwal GB, Hamblin MR. Cell death pathways in photodynamic therapy of cancer. Cancers. 2011 Jun 1;3(2):2516-2539. https://doi.org/10.3390/cancers3022516
Mroz, Pawel ; Yaroslavsky, Anastasia ; Kharkwal, Gitika B. ; Hamblin, Michael R. / Cell death pathways in photodynamic therapy of cancer. In: Cancers. 2011 ; Vol. 3, No. 2. pp. 2516-2539.
@article{aee7c7846685424895116835ae1d48c5,
title = "Cell death pathways in photodynamic therapy of cancer",
abstract = "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.",
keywords = "Apoptosis, Autophagy, Cancer, Cell death, Necrosis, Photodynamic therapy",
author = "Pawel Mroz and Anastasia Yaroslavsky and Kharkwal, {Gitika B.} and Hamblin, {Michael R.}",
year = "2011",
month = "6",
day = "1",
doi = "10.3390/cancers3022516",
language = "English (US)",
volume = "3",
pages = "2516--2539",
journal = "Cancers",
issn = "2072-6694",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "2",

}

TY - JOUR

T1 - Cell death pathways in photodynamic therapy of cancer

AU - Mroz, Pawel

AU - Yaroslavsky, Anastasia

AU - Kharkwal, Gitika B.

AU - Hamblin, Michael R.

PY - 2011/6/1

Y1 - 2011/6/1

N2 - 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.

AB - 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.

KW - Apoptosis

KW - Autophagy

KW - Cancer

KW - Cell death

KW - Necrosis

KW - Photodynamic therapy

UR - http://www.scopus.com/inward/record.url?scp=79959724644&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79959724644&partnerID=8YFLogxK

U2 - 10.3390/cancers3022516

DO - 10.3390/cancers3022516

M3 - Review article

VL - 3

SP - 2516

EP - 2539

JO - Cancers

JF - Cancers

SN - 2072-6694

IS - 2

ER -