Potential mechanisms involved in resistant phenotype of mcf-7 breast carcinoma cells to ionizing radiation induced apoptosis
文献类型:期刊论文
作者 | Wang, Yan-ling1,2,3; Zhang, Hong1,2; Li, Ning1,2,3; Wang, Xiao-hu4; Hao, Ji-fang1,2; Zhao, Wei-ping1,2,3 |
刊名 | Nuclear instruments & methods in physics research section b-beam interactions with materials and atoms
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出版日期 | 2009-03-01 |
卷号 | 267期号:6页码:1001-1006 |
关键词 | Brca1 Phosphorylation Ionizing radiation (ir) P21 Bax Bcl-2 |
ISSN号 | 0168-583X |
DOI | 10.1016/j.nimb.2009.02.014 |
通讯作者 | Zhang, hong(zhangh@impcas.ac.cn) |
英文摘要 | In the present study, we investigated the mechanisms of apoptosis resistance and the roles of the phosphorylation of brca1, p21, the bax/bcl-2 protein ratio and cell cycle arrest in ir-induced apoptosis in mcf-7 cells. x-irradiation, in particular at low dose (1 gy), but not carbon ion irradiation, had a significant anti proliferative effect on the growth of mcf-7 cells. i gy x-irradiation resulted in g1 and g2 phase arrest, but 4 gy induced a significant g1 block. in contrast, carbon ion irradiation resulted in a significant accumulation in the g2 phase. concomitant with the phosphorylation of h2ax induced by dna damage, carbon ion irradiation resulted in all approximately 1.9-2.8-fold increase in the phosphorylation of brca1 on serine residue 1524, significantly greater than that detected for x-irradiation. carbon ion irradiation caused a dramatic increase in p21 expression and drastic decrease in bax expression compared with x-irradiation. the data implicated that phospholylation of brca1 on serine residue 1524 might, at least partially, induce p21 expression but repress bax expression. together, our results suggested that the phosphorylation of brca1 at ser-1524 might contribute to the g2 phase arrest and might be an upstream signal involved in preventing apoptosis signal via upregulation of p21 and downregulation of the bax/bcl-2 ratio. (c) 2009 elsevier b.v. all lights reserved. |
WOS关键词 | DNA-DAMAGE RESPONSE ; DOUBLE-STRANDED BREAKS ; IN-VIVO ; HOMOLOGOUS RECOMBINATION ; ATAXIA-TELANGIECTASIA ; GENE-EXPRESSION ; HISTONE H2AX ; BCL-2 FAMILY ; BRCA1 ; ARREST |
WOS研究方向 | Instruments & Instrumentation ; Nuclear Science & Technology ; Physics |
WOS类目 | Instruments & Instrumentation ; Nuclear Science & Technology ; Physics, Atomic, Molecular & Chemical ; Physics, Nuclear |
语种 | 英语 |
WOS记录号 | WOS:000265815200034 |
出版者 | ELSEVIER SCIENCE BV |
URI标识 | http://www.irgrid.ac.cn/handle/1471x/2402202 |
专题 | 中国科学院大学 |
通讯作者 | Zhang, Hong |
作者单位 | 1.Chinese Acad Sci, Inst Modern Phys, Lanzhou 730000, Peoples R China 2.Key Lab Heavy Ion Radiat Med Gansu Prov, Lanzhou 730000, Peoples R China 3.Chinese Acad Sci, Grad Sch, Beijing 100039, Peoples R China 4.Gansu Tumor Hosp, Dept Radiotherapy, Lanzhou 730050, Peoples R China |
推荐引用方式 GB/T 7714 | Wang, Yan-ling,Zhang, Hong,Li, Ning,et al. Potential mechanisms involved in resistant phenotype of mcf-7 breast carcinoma cells to ionizing radiation induced apoptosis[J]. Nuclear instruments & methods in physics research section b-beam interactions with materials and atoms,2009,267(6):1001-1006. |
APA | Wang, Yan-ling,Zhang, Hong,Li, Ning,Wang, Xiao-hu,Hao, Ji-fang,&Zhao, Wei-ping.(2009).Potential mechanisms involved in resistant phenotype of mcf-7 breast carcinoma cells to ionizing radiation induced apoptosis.Nuclear instruments & methods in physics research section b-beam interactions with materials and atoms,267(6),1001-1006. |
MLA | Wang, Yan-ling,et al."Potential mechanisms involved in resistant phenotype of mcf-7 breast carcinoma cells to ionizing radiation induced apoptosis".Nuclear instruments & methods in physics research section b-beam interactions with materials and atoms 267.6(2009):1001-1006. |
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来源:中国科学院大学
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