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JNK信号通路在δ氨基酮戊酸-光动力疗法诱导SW480细胞凋亡中的作用机制 被引量:2

Role of the c-Jun N-terminal kinase signaling pathway in SW480 cell apoptosis in response to 5-aminolevulinic acid-based photodynamic therapy
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摘要 目的:探讨JNK信号通路在δ氨基酮戊酸(ALA)-光动力疗法((PDT)诱导SW480细胞凋亡中的作用.方法:将SW480细胞分为空白对照组、激光照射组、ALA组及ALA-PDT组,Western blot检测各组细胞c-Jun氨基末端激酶(JNK)的表达;用SP600125(JNK抑制剂)预孵育ALA-PDT组细胞,Western blot检测各组细胞的多聚(ADP-核糖)聚合酶(PARP)的表达.结果:磷酸化JNK在空白对照组、激光照射组及ALA组几乎无表达,ALA-PDT后30-90 min细胞表达显著高于空白对照组、激光照射组及ALA组(F=12.314,P<0.001),其中ALA-PDT后60及90 min的磷酸化JNK表达显著高于ALA-PDT后30 min(F=9.782,P<0.001),各组细胞总的JNK表达无显著差异.JNK的激活能抑制ALA-PDT诱导SW480细胞凋亡.结论:JNK信号通路的激活抑制ALA-PDT诱导SW480细胞凋亡;JNK通路可能成为增强ALA-PDT治疗结肠癌的新靶点. AIM:To investigate the role of the c-Jun N-terminal kinase(JNK)signaling pathway in SW480 cell apoptosis in response to 5-aminolevulinic acid(ALA)-based photodynamic therapy(PDT).METHODS:SW480 cells were divided into con-trol group,laser irradiation group,ALA group and ALA-PDT group.Western blot was used to detect expression of JNK in each group.SW480 cells in ALA-PDT group were preincubated with SP600125(JNK inhibitor).Western blot was usedto detect expression of PARP in each group.RESULTS:JNK phosphorylation almost had no expression in control group,light group or ALA group.JNK phosphorylation of SW480 cells at 30,60 and 90 min after ALA-PDT was signifi-cantly increased than that of control group,light group or ALA group(F=12.314,P〈0.001).Phosphorylated JNK expression was signifi-cantly higher at 60 min and 90 min after ALA-PDT than at 30 min after ALA-PDT(F=9.782,P〈0.001).The expression of total JNK of all groups had no significant difference.The activa-tion of JNK inhibited apoptosis of SW480 cells in response to ALA-PDT.CONCLUSION:AActivation of JNK signaling pathway inhibits SW480 cell apoptosis after ALA-PDT.JNK signaling pathway may become a new target,which will enhance anticancer treatment of ALA-PDT for colon carcinoma.
出处 《世界华人消化杂志》 CAS 北大核心 2008年第33期3792-3795,共4页 World Chinese Journal of Digestology
关键词 δ氨基酮戊酸 光动力疗法 结肠癌细胞 细胞凋亡 JNK信号通路 Aminolevulinic acid Photodynamic therapy Colon carcinoma Apoptosis the c-Jun N-terminal kinase signaling pathway
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参考文献17

  • 1Johansen LS. [Photodynamic therapy. A new method for the treatment of cancer] Ugeskr Laeger 1999; 161:3992-3995
  • 2Assefa Z, Vantieghem A, Declercq W, Vandenabeele P, Vandenheede JR, Merlevede W, de Witte P, Agostinis P. The activation of the c-Jun N-terminal kinase and p38 mitogen-activated protein kinase signaling pathways protects HeLa cells from apoptosis following photodynamic therapy with hypericin. J Biol Chem 1999; 274:8788-8796
  • 3Xue L, He J, Oleinick NL. Promotion of photodynamic therapy-induced apoptosis by stress kinases. Cell Death Differ 1999; 6:855-864
  • 4Chert YR, Meyer CF, Tan TH. Persistent activation of c-Jun N-terminal kinase 1 (JNK1) in gamma radiation-induced apoptosis. J Biol Chem 1996; 271: 631-634
  • 5Kick G, Messer G, Plewig G, Kind P, Goetz AE. Strong and prolonged induction of c-jun and c-fos proto-oncogenes by photodynamic therapy. Br J Cancer 1996; 74:30-36
  • 6Klotz LO, Fritsch C, Briviba K, Tsacmacidis N, Schliess F, Sies H. Activation of JNK and p38 but not ERK MAP kinases in human skin cells by 5-aminolevulinate-photodynamic therapy. Cancer Res 1998; 58:4297-4300
  • 7Peng Q, Warloe T, Moan J, Godal A, Apricena F, Giercksky KE, Nesland JM. Antitumor effect of 5-aminolevulinic acid-mediated photodynamic therapy can be enhanced by the use of a low dose of photofrin in human tumor xenografts. Cancer Res 2001; 61:5824-5832
  • 8Niedre M, Patterson MS, Wilson BC. Direct near-infrared luminescence detection of singlet oxygen generated by photodynamic therapy in cells in vitro and tissues in vivo. Photochem Photobiol 2002; 75: 382-391
  • 9Bartosova J, Hrkal Z. Accumulation of protoporphyrin-Ⅸ(PpⅨ) in leukemic cell lines following induction by 5-aminolevulinic acid (ALA). Comp Biochem Physiol C Toxicol Pharmacol 2000; 126:245-252
  • 10Dougherty TJ, Gomer CJ, Henderson BW, Jori G, Kessel D, Korbelik M, Moan J, Peng Q. Photodynamic therapy. J Natl Cancer Inst 1998; 90: 889-905

二级参考文献1

  • 1Tajiri H,Hayakawa A,Matsumoto Y,et al.Changes in intracellular Ca^2+ concentrations related to PDT-induced apoptosis in photosensitized human cancer cell.Cancer Lett,1998,128:205-210.?A

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  • 1卫生部医政司 结直肠癌诊疗规范专家工作组.结直肠癌诊疗规范(2010年)[J].中华胃肠外科杂志,2010,:865-875.
  • 2Hibi M, Lin A, Smeal T, Minden A, Karin M. Identification of an oncoproteinand UV-responsive protein kinase that binds and potentiates the c-Jun activation domain. Genes Dev 1993; 7:2135-2148.
  • 3Johnson GL, Nakamura K. The c-jun kinase/stressactivated pathway: regulation, function and role in human disease. Biochim Biophys Acta 2007; 1773: 1341-1348.
  • 4Lin MT, Beal MF. Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases. Nature 2006; 448:787-795.
  • 5Mori Y, Gotoh Y. [Role of the JNK signaling pathway]. Tanpakushitsu Kakusan Koso 2008; 53:1252-1257.
  • 6Wagner EF, Nebreda AR. Signal integration by JNK and p38 MAPK pathways in cancer development. Nat Rev Cancer 2009; 9:537-549.
  • 7Heasley LE, Han SY. JNK regulation of oncogenesis. Mol Cells 2006; 21:167-173.
  • 8Uhlirova M, Jasper H, Bohmann D. Non-cell-autonomous induction of tissue overgrowth by JNK/Ras cooperation in a Drosophila tumor model. Proc Natl Acad Sci U S A 2005; 102:13123-13128.
  • 9Nateri AS, Spencer-Dene B, Behrens A. Interaction of phosphorylated c-Jun with TCF4 regulates intestinal cancer development. Nature 2005; 437:281-285.
  • 10She QB, Chen N, Bode AM, Flavell RA, Dong Z. Deficiency of c-Jun-NH(2)-terminal kinase-1 in mice enhances skin tumor development by 12-0tetradecanoylphorbol-13-acetate. Cancer Res 2002; 62:1343-1348.

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