摘要
原文 | 英語 |
---|---|
期刊 | Molecular Cancer |
卷 | 9 |
DOIs | |
出版狀態 | 已發佈 - 2010 |
對外發佈 | 是 |
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於: Molecular Cancer, 卷 9, 2010.
研究成果: 雜誌貢獻 › 文章 › 同行評審
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TY - JOUR
T1 - 5-ALA mediated photodynamic therapy induces autophagic cell death via AMP-activated protein kinase
AU - Ji, Hong-Tai
AU - Chien, Li-Ting
AU - Lin, Yu-Hsin
AU - Chien, Hsiung-Fei
AU - Chen, Chin-Tin
N1 - 被引用次數:24 Export Date: 16 March 2016 CODEN: MCOAC 通訊地址: Chen, C.-T.; Department of Biochemical Science and Technology, National Taiwan University, Taipei 106, Taiwan; 電子郵件: [email protected] 化學物質/CAS: aminolevulinic acid, 106-60-5; caspase 3, 169592-56-7; caspase 9, 180189-96-2; hydroxymethylglutaryl coenzyme A reductase kinase, 172522-01-9, 72060-32-3; mitogen activated protein kinase, 142243-02-5; stress activated protein kinase, 155215-87-5; adenylate kinase, 9013-02-9; Adenylate Kinase, 2.7.4.3; Aminolevulinic Acid, 106-60-5; Photosensitizing Agents 製造商: Sigma, United States 參考文獻: Dougherty, T.J., Gomer, C.J., Henderson, B.W., Jori, G., Kessel, D., Korbelik, M., Moan, J., Peng, Q., Photodynamic therapy (1998) J Natl Cancer Inst, 90, pp. 889-905. , 10.1093/jnci/90.12.889, 9637138; Dolmans, D.E., Fukumura, D., Jain, R.K., Photodynamic therapy for cancer (2003) Nat Rev Cancer, 3, pp. 380-387. , 10.1038/nrc1071, 12724736; Gomer, C.J., Rucker, N., Ferrario, A., Wong, S., Properties and applications of photodynamic therapy (1989) Radiat Res, 120, pp. 1-18. , 10.2307/3577632, 2678224; Almeida, R.D., Manadas, B.J., Carvalho, A.P., Duarte, C.B., Intracellular signaling mechanisms in photodynamic therapy (2004) Biochim Biophys Acta, 1704, pp. 59-86; Buytaert, E., Dewaele, M., Agostinis, P., Molecular effectors of multiple cell death pathways initiated by photodynamic therapy (2007) Biochim Biophys Acta, 1776, pp. 86-107; Gardner, L.C., Smith, S.J., Cox, T.M., Biosynthesis of delta-aminolevulinic acid and the regulation of heme formation by immature erythroid cells in man (1991) J Biol Chem, 266, pp. 22010-22018; Hardie, D.G., Carling, D., The AMP-activated protein kinase--fuel gauge of the mammalian cell? 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PY - 2010
Y1 - 2010
N2 - Photodynamic therapy (PDT) has been developed as an anticancer treatment, which is based on the tumor-specific accumulation of a photosensitizer that induces cell death after irradiation of light with a specific wavelength. Depending on the subcellular localization of the photosensitizer, PDT could trigger various signal transduction cascades and induce cell death such as apoptosis, autophagy, and necrosis. In this study, we report that both AMP-activated protein kinase (AMPK) and mitogen-activated protein kinase (MAPK) signaling cascades are activated following 5-aminolevulinic acid (ALA)-mediated PDT in both PC12 and CL1-0 cells. Although the activities of caspase-9 and -3 are elevated, the caspase inhibitor zVAD-fmk did not protect cells against ALA-PDT-induced cell death. Instead, autophagic cell death was found in PC12 and CL1-0 cells treated with ALA-PDT. Most importantly, we report here for the first time that it is the activation of AMPK, but not MAPKs that plays a crucial role in mediating autophagic cell death induced by ALA-PDT. This novel observation indicates that the AMPK pathway play an important role in ALA-PDT-induced autophagy. © 2010 Ji et al; licensee BioMed Central Ltd.
AB - Photodynamic therapy (PDT) has been developed as an anticancer treatment, which is based on the tumor-specific accumulation of a photosensitizer that induces cell death after irradiation of light with a specific wavelength. Depending on the subcellular localization of the photosensitizer, PDT could trigger various signal transduction cascades and induce cell death such as apoptosis, autophagy, and necrosis. In this study, we report that both AMP-activated protein kinase (AMPK) and mitogen-activated protein kinase (MAPK) signaling cascades are activated following 5-aminolevulinic acid (ALA)-mediated PDT in both PC12 and CL1-0 cells. Although the activities of caspase-9 and -3 are elevated, the caspase inhibitor zVAD-fmk did not protect cells against ALA-PDT-induced cell death. Instead, autophagic cell death was found in PC12 and CL1-0 cells treated with ALA-PDT. Most importantly, we report here for the first time that it is the activation of AMPK, but not MAPKs that plays a crucial role in mediating autophagic cell death induced by ALA-PDT. This novel observation indicates that the AMPK pathway play an important role in ALA-PDT-induced autophagy. © 2010 Ji et al; licensee BioMed Central Ltd.
KW - aminolevulinic acid
KW - caspase 3
KW - caspase 9
KW - hydroxymethylglutaryl coenzyme A reductase kinase
KW - mitogen activated protein kinase
KW - mitogen activated protein kinase p38
KW - stress activated protein kinase
KW - adenylate kinase
KW - photosensitizing agent
KW - animal cell
KW - article
KW - autophagy
KW - cancer cell
KW - controlled study
KW - DNA fragmentation
KW - enzyme activation
KW - human
KW - human cell
KW - mitochondrial membrane potential
KW - nonhuman
KW - oxidative stress
KW - photodynamic therapy
KW - survival rate
KW - animal
KW - drug effect
KW - genetic transfection
KW - immunoblotting
KW - metabolism
KW - methodology
KW - mitochondrion
KW - pathology
KW - photochemotherapy
KW - physiology
KW - rat
KW - signal transduction
KW - Adenylate Kinase
KW - Aminolevulinic Acid
KW - Animals
KW - Autophagy
KW - DNA Fragmentation
KW - Immunoblotting
KW - MAP Kinase Signaling System
KW - Membrane Potential, Mitochondrial
KW - Mitochondria
KW - Oxidative Stress
KW - Photochemotherapy
KW - Photosensitizing Agents
KW - Rats
KW - Signal Transduction
KW - Transfection
U2 - 10.1186/1476-4598-9-91
DO - 10.1186/1476-4598-9-91
M3 - Article
SN - 1476-4598
VL - 9
JO - Molecular Cancer
JF - Molecular Cancer
ER -