Cell proliferation and cell cycle alterations in oesophageal p53-mutated cancer cells treated with cisplatin in combination with photodynamic therapy

被引:28
作者
Compagnin, C. [2 ]
Mognato, M. [2 ]
Celotti, L. [1 ,2 ]
Canti, G. [3 ]
Palumbo, G. [4 ]
Reddi, E. [2 ]
机构
[1] Ist Nazl Fis Nucl, Lab Nazl Legnaro, Padua, Italy
[2] Univ Padua, Dipartimento Biol, I-35131 Padua, Italy
[3] Univ Milan, Dipartimento Farmacol, Milan, Italy
[4] Univ Naples Federico 2, Dipartimento Biol & Patol Cellulare & Mol, Naples, Italy
关键词
HIGH-GRADE DYSPLASIA; DNA-DAMAGE; P53; STATUS; MITOCHONDRIAL-MEMBRANE; BARRETTS-ESOPHAGUS; INDUCED APOPTOSIS; ANTICANCER DRUGS; MURINE TUMORS; IN-VITRO; DEATH;
D O I
10.1111/j.1365-2184.2010.00673.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Objectives: The major goal of anti-cancer therapies is selective destruction of tumour cells with minimum side effects on normal cells. Towards this aim, combination of different therapeutic modalities has been evaluated for improving control of neoplastic diseases and quality of life for the patient. Photodynamic therapy (PDT) is a procedure for treatment of various types of cancer, but its combination with other established treatments has not been evaluated in detail. We have used KYSE-510 cells from a human oesophageal carcinoma as an in vitro model to investigate whether cisplatin (CDDP) could be combined with PDT to increase cell death with respect to single treatments. Materials and methods: p53-mutated KYSE-510 cells were treated with CDDP alone or in combination with PDT. Analyses of cell viability, cell cycle progression and apoptosis induction were carried out at specific times after treatments. Results: Decrease in cell viability, cell cycle arrest at the G(2)/M- and S-phases boundary, and apoptosis induction were observed after single and combined treatments. Conclusions: Our results show that low CDDP doses (0.25-1 mu m) induce cell mortality and cell cycle perturbation, which were more evident when given in combination with PDT, but in contrast to work of other authors no synergistic activity was found. Apoptosis occurred via intrinsic pathways in treated cells, although it did not represent the predominant mode of cell death.
引用
收藏
页码:262 / 274
页数:13
相关论文
共 54 条
[1]   Apoptosis-associated release of Smac/DIABLO from mitochondria requires active caspases and is blocked by Bcl-2 [J].
Adrain, C ;
Creagh, EM ;
Martin, SJ .
EMBO JOURNAL, 2001, 20 (23) :6627-6636
[2]   Bax is present as a high molecular weight oligomer/complex in the mitochondrial membrane of apoptotic cells [J].
Antonsson, B ;
Montessuit, S ;
Sanchez, B ;
Martinou, JC .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (15) :11615-11623
[3]   ACTIVATION OF PROGRAMMED CELL-DEATH (APOPTOSIS) BY CISPLATIN, OTHER ANTICANCER DRUGS, TOXINS AND HYPERTHERMIA [J].
BARRY, MA ;
BEHNKE, CA ;
EASTMAN, A .
BIOCHEMICAL PHARMACOLOGY, 1990, 40 (10) :2353-2362
[4]  
BEREK JS, 1989, OBSTET GYNECOL, V74, P663
[5]  
Bergman AM, 1996, CLIN CANCER RES, V2, P521
[6]   Kinetic analysis of the cis-diamminedichloroplatinum(II)-cysteine reaction: Implications to the extent of platinum-DNA binding [J].
Bose, RN ;
Ghosh, SK ;
Moghaddas, S .
JOURNAL OF INORGANIC BIOCHEMISTRY, 1997, 65 (03) :199-205
[7]   Cell proliferation, apoptosis and mitochondrial damage in rat B50 neuronal cells after cisplatin treatment [J].
Bottone, M. G. ;
Soldani, C. ;
Veneroni, P. ;
Avella, D. ;
Pisu, M. ;
Bernocchi, G. .
CELL PROLIFERATION, 2008, 41 (03) :506-520
[8]   The present and future role of photodynamic therapy in cancer treatment [J].
Brown, SB ;
Brown, EA ;
Walker, I .
LANCET ONCOLOGY, 2004, 5 (08) :497-508
[9]   Antitumor efficacy of the combination of photodynamic therapy and chemotherapy in murine tumors [J].
Canti, G ;
Nicolin, A ;
Cubeddu, R ;
Taroni, P ;
Bandieramonte, G ;
Valentini, G .
CANCER LETTERS, 1998, 125 (1-2) :39-44
[10]   Oxidative stress induction by T-2 toxin causes DNA damage and triggers apoptosis via caspase pathway in human cervical cancer cells [J].
Chaudhari, Manjari ;
Jayaraj, R. ;
Bhaskar, A. S. B. ;
Rao, P. V. Lakshmana .
TOXICOLOGY, 2009, 262 (02) :153-161