Document Detail


Isolation and characterization of radiation-resistant lung cancer D6-R cell line.
MedLine Citation:
PMID:  18837299     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: To isolate an isogenic radioresistant cancer cell line after fractioned X-ray radiation and characterize the resistant cells. METHODS: D6 cells were exposed to repeated X-ray irradiation, and after a total dose of 5200 cGy in 8 fractions, a radioresistant monoclone D6-R was obtained. The radiosensitivity and drug sensitivity of the novel radioresistant D6-R cells, together with their parent D6 cells, were measured using clonogenic assay and MTT assay respectively. Cell cycle distribution was analyzed by flow cytometry. Fluorescence microscopy and flow cytometry were applied for apoptosis detection. Comet assay was used for the detection of DNA damage and repair. RESULTS: D6-R cells showed higher and broader initial shoulder (D0=2.08 Gy, Dq=1.64 Gy, N=2.20) than the parent D6 cells (D0=1.84 Gy, Dq=0.34 Gy, N=1.20). They were 1.65-fold more radioresistant than D6 cells in terms of SF2 (63% vs 38%) and were more resistant to ADM (3.15-fold) and 5-FU (3.86-fold) as compared with the latter. It was found that D6-R cells had higher fractions of cells in S phase (53.4% vs 37.8%) and lower fractions of cells in G1 (44.1% vs 57.2%) and G2-M phase (2.5% vs 5%). There was no difference in radiation-induced apoptosis between D6-R and D6 cells. D6-R cells showed less initial DNA damage and increased capacity in DNA repair after irradiation, as compared with the parent cells. CONCLUSIONS: D6-R cells have been isolated by exposing the parental D6 cells to repeated irradiation. The difference in cell cycle pattern together with the induction and repair of DNA damage might, at least partially, explain the mechanism of the radioresistance.
Authors:
Qi-Chun Wei; Li Shen; Shu Zheng; Yong-Liang Zhu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Biomedical and environmental sciences : BES     Volume:  21     ISSN:  0895-3988     ISO Abbreviation:  Biomed. Environ. Sci.     Publication Date:  2008 Aug 
Date Detail:
Created Date:  2008-10-07     Completed Date:  2008-10-16     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8909524     Medline TA:  Biomed Environ Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  339-44     Citation Subset:  IM    
Affiliation:
Ministry of Education Key Laboratory of Cancer Prevention and Intervention, Zhejiang University, Hangzhou 310009, Zhejiang, China. Qichun_Wei@zju.edu.cn
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MeSH Terms
Descriptor/Qualifier:
Apoptosis
Carcinoma, Non-Small-Cell Lung / pathology*,  radiotherapy*
Cell Cycle
Cell Line, Tumor
DNA Damage
DNA Repair
Flow Cytometry
Humans
Lung Neoplasms / pathology*
Microscopy, Fluorescence

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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