ANTICANCER EFFECT OF PHOTODYNAMIC THERAPY WITH HEXENYL ESTER OF 5-AMINOLEVULINIC ACID IN ORAL SQUAMOUS CELL CARCINOMA

被引:15
作者
Moon, Yeon-Hee [1 ]
Park, Jong-Hwan [1 ]
Kim, Soo-A [2 ]
Lee, Jee-Bum [3 ]
Ahn, Sang-Gun [1 ]
Yoon, Jung-Hoon [1 ]
机构
[1] Chosun Univ, Sch Dent, Dept Pathol, Kwangju 501759, South Korea
[2] Dongguk Univ, Coll Oriental Med, Dept Biochem, Gyungju 780714, South Korea
[3] Chonnam Natl Univ, Sch Med, Dept Dermatol, Kwangju 501757, South Korea
来源
HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND NECK | 2010年 / 32卷 / 09期
关键词
5-aminolevulinic acid (ALA); protoporphyrin IX (PpIX); human oral squamous cell carcinoma; reactive oxygen species; apoptosis; AMINOLEVULINIC ACID; ICE/CED-3; PROTEASE; DNA-DAMAGE; IN-VITRO; POLY(ADP-RIBOSE); CANCER; IDENTIFICATION; PHOTOTOXICITY; DERIVATIVES; MECHANISMS;
D O I
10.1002/hed.21301
中图分类号
R76 [耳鼻咽喉科学];
学科分类号
100213 ;
摘要
Background. Five-aminolaevulinic acid (ALA) and its derivatives act as precursors of the photosensitizer protoporphyrin IX (PpIX). In this study, the effect of photodynamic therapy (PDT) with hexenyl ester of ALA (ALA-hx) was examined in a human oral squamous cell carcinoma, YD10B cells. Methods. PpIX accumulation and mRNA expression of coproporphyrinogen oxidase (CPO) by ALA and ALA-hx was examined. Cell viability was examined by MTT assay and the molecular mechanism was investigated. Results. The PpIX synthesis and mRNA expression of CPO was much higher in the cells treated with ALA-hx than ALA. At the concentration that PDT with ALA did not affect cell growth, ALA-hx PDT effectively produced reactive oxygen species (ROS) and suppressed cell growth. Growth inhibition by ALA-hx PDT was due to mitochondrial-dependent apoptosis. Conclusion. Our results suggest that ALA-hx PDT effectively induced apoptosis of YD-10B cells and can be considered as a therapeutic alternative for oral cancer. (c) 2009 Wiley Periodicals, Inc. Head Neck 32: 1136-1142, 2010
引用
收藏
页码:1136 / 1142
页数:7
相关论文
共 30 条
[1]   Human ICE/CED-3 protease nomenclature [J].
Alnemri, ES ;
Livingston, DJ ;
Nicholson, DW ;
Salvesen, G ;
Thornberry, NA ;
Wong, WW ;
Yuan, JY .
CELL, 1996, 87 (02) :171-171
[2]   SYMPOSIUM - CELLULAR-RESPONSE TO DNA DAMAGE - THE ROLE OF POLY(ADP-RIBOSE) - POLY(ADP-RIBOSE) IN THE CELLULAR-RESPONSE TO DNA DAMAGE [J].
BERGER, NA .
RADIATION RESEARCH, 1985, 101 (01) :4-15
[3]   IDENTIFICATION OF MINIMAL SIZE REQUIREMENTS OF DNA FOR ACTIVATION OF POLY(ADP-RIBOSE) POLYMERASE [J].
BERGER, NA ;
PETZOLD, SJ .
BIOCHEMISTRY, 1985, 24 (16) :4352-4355
[4]  
Brunner H, 2003, PHOTOCHEM PHOTOBIOL, V78, P481, DOI 10.1562/0031-8655(2003)078<0481:NAAEPP>2.0.CO
[5]  
2
[6]   Mechanisms in photodynamic therapy: part one-photosensitizers, photochemistry and cellular localization [J].
Castano, Ana P. ;
Demidova, Tatiana N. ;
Hamblin, Michael R. .
PHOTODIAGNOSIS AND PHOTODYNAMIC THERAPY, 2004, 1 (04) :279-293
[7]   Head and neck cancer: past, present and future [J].
Chin, David ;
Boyle, Glen M. ;
Porceddu, Sandro ;
Theile, David R. ;
Parsons, Peter G. ;
Coman, William B. .
EXPERT REVIEW OF ANTICANCER THERAPY, 2006, 6 (07) :1111-1118
[8]   Proteases to die for [J].
Cryns, V ;
Yuan, JY .
GENES & DEVELOPMENT, 1998, 12 (11) :1551-1570
[9]  
Frimberger AE, 1998, CLIN CANCER RES, V4, P2207
[10]  
Gerscher S, 2000, PHOTOCHEM PHOTOBIOL, V72, P569, DOI 10.1562/0031-8655(2000)072<0569:COTPAP>2.0.CO