Photoirradiation after aminolevulinic acid treatment suppresses cancer cell proliferation through the HO-1/p21 pathway.


Journal

Photodiagnosis and photodynamic therapy
ISSN: 1873-1597
Titre abrégé: Photodiagnosis Photodyn Ther
Pays: Netherlands
ID NLM: 101226123

Informations de publication

Date de publication:
Dec 2019
Historique:
received: 05 06 2019
revised: 09 07 2019
accepted: 26 07 2019
pubmed: 14 8 2019
medline: 2 5 2020
entrez: 13 8 2019
Statut: ppublish

Résumé

Photodynamic therapy (PDT) and diagnosis (PDD) using 5-aminolevulinic acid (ALA) to control the production of an intracellular photosensitizer, protoporphyrin IX (PpIX), are in common clinical use. Although various studies have been published regarding cell death analysis after photoirradiation by ALA-PDT, the changes in gene expressions induced by it are yet unclear. Here, we focused on studying gene expression and cell proliferation changes in cancer cells that survive photoirradiation. HEK293 human embryonic kidney cells, MKN45 human gastric cells, and PC-3 human prostate cancer cells were selected for this research. Cell viability was measured using trypan blue and MTT assays. ALA-PDT experiments were performed using a calibrated LED irradiation module. Furthermore, mRNA and protein gene expression analysis were performed using our previously reported methods. mRNAs of PAI-1, HO-1, and p21 were upregulated after photoirradiation of HEK293, which was suppressed by N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger. Primer array results in PC-3 cells and p21 and Ki-67 expression results in both PC-3 and MKN45 cells suggested that photoirradiation suppressed cell proliferation. Cell numbers post-photoirradiation revealed that the proliferation of surviving cells was suppressed in PC-3 and MKN45 cells. ALA-PDD or ALA-PDT can result in rapid ROS-induced cell death and may decrease long-term recurrence rates through several pathways including the HO-1/p21 pathway.

Sections du résumé

BACKGROUND BACKGROUND
Photodynamic therapy (PDT) and diagnosis (PDD) using 5-aminolevulinic acid (ALA) to control the production of an intracellular photosensitizer, protoporphyrin IX (PpIX), are in common clinical use. Although various studies have been published regarding cell death analysis after photoirradiation by ALA-PDT, the changes in gene expressions induced by it are yet unclear. Here, we focused on studying gene expression and cell proliferation changes in cancer cells that survive photoirradiation.
METHODS METHODS
HEK293 human embryonic kidney cells, MKN45 human gastric cells, and PC-3 human prostate cancer cells were selected for this research. Cell viability was measured using trypan blue and MTT assays. ALA-PDT experiments were performed using a calibrated LED irradiation module. Furthermore, mRNA and protein gene expression analysis were performed using our previously reported methods.
RESULTS RESULTS
mRNAs of PAI-1, HO-1, and p21 were upregulated after photoirradiation of HEK293, which was suppressed by N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger. Primer array results in PC-3 cells and p21 and Ki-67 expression results in both PC-3 and MKN45 cells suggested that photoirradiation suppressed cell proliferation. Cell numbers post-photoirradiation revealed that the proliferation of surviving cells was suppressed in PC-3 and MKN45 cells.
CONCLUSION CONCLUSIONS
ALA-PDD or ALA-PDT can result in rapid ROS-induced cell death and may decrease long-term recurrence rates through several pathways including the HO-1/p21 pathway.

Identifiants

pubmed: 31404677
pii: S1572-1000(19)30284-4
doi: 10.1016/j.pdpdt.2019.07.021
pii:
doi:

Substances chimiques

Cyclin-Dependent Kinase Inhibitor p21 0
Photosensitizing Agents 0
RNA, Messenger 0
Reactive Oxygen Species 0
Aminolevulinic Acid 88755TAZ87
Heme Oxygenase-1 EC 1.14.14.18

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

10-17

Informations de copyright

Copyright © 2019. Published by Elsevier B.V.

Auteurs

Taku Nakayama (T)

Department of Bioengineering, School of Life Science and Technology, Tokyo Institute of Technology, Japan; Center for Photodynamic Medicine, Kochi Medical School, Japan.

Tatsuya Kobayashi (T)

Department of Bioengineering, School of Life Science and Technology, Tokyo Institute of Technology, Japan.

Otsuka Shimpei (O)

Department of Bioengineering, School of Life Science and Technology, Tokyo Institute of Technology, Japan.

Hideo Fukuhara (H)

Center for Photodynamic Medicine, Kochi Medical School, Japan; Department of Urology, Kochi Medical School, Japan.

Tsutomu Namikawa (T)

Center for Photodynamic Medicine, Kochi Medical School, Japan; Department of Surgery I, Kochi Medical School, Japan.

Keiji Inoue (K)

Center for Photodynamic Medicine, Kochi Medical School, Japan; Department of Urology, Kochi Medical School, Japan.

Kazuhiro Hanazaki (K)

Center for Photodynamic Medicine, Kochi Medical School, Japan; Department of Surgery I, Kochi Medical School, Japan.

Kiwamu Takahashi (K)

SBI Pharmaceuticals Co., Ltd., Japan.

Motowo Nakajima (M)

SBI Pharmaceuticals Co., Ltd., Japan.

Tohru Tanaka (T)

SBI Pharmaceuticals Co., Ltd., Japan.

Shun-Ichiro Ogura (SI)

Department of Bioengineering, School of Life Science and Technology, Tokyo Institute of Technology, Japan; Center for Photodynamic Medicine, Kochi Medical School, Japan. Electronic address: sogura@bio.titech.ac.jp.

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Classifications MeSH