Liu Xiguang,Zhang Hongjun,Song Tingting,Li Jingdong.The effect of apoptosis-2 ligand on irradiation-induced apoptosis in lung adenocarcinima H1975 cells resistant to EGFR-TKI[J].Chinese Journal of Radiological Medicine and Protection,2016,36(6):424-429
The effect of apoptosis-2 ligand on irradiation-induced apoptosis in lung adenocarcinima H1975 cells resistant to EGFR-TKI
Received:September 03, 2015  
DOI:10.3760/cma.j.issn.0254-5098.2016.06.005
KeyWords:Apoptosis-2 ligand  Apoptosis  Irradiation  H1975 cell-line
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Author NameAffiliation
Liu Xiguang Department of Oncology, Affiliated Hospital of Qingdao University, Qingdao 266003, China 
Zhang Hongjun Department of Oncology, Affiliated Hospital of Qingdao University, Qingdao 266003, China 
Song Tingting Department of Oncology, Qingdao Central Hospital, Qingdao 266042, China 
Li Jingdong Department of Oncology, Linyi People's Hospital, Linyi 276003, China 
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Abstract::
      Objective To investigate whether the apoptosis-2 ligand (Apo-2L), known as tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), could enhance irradiation-induced apoptosis in lung adenocarcinima H1975 cells that are resistant to the epithelial growth factor receptor (EGFR)-TKI. Methods Adenocarcinima H1975 cells were randomly divided into four groups:the control group, Apo-2L group, irradiation group, and both Apo-2L and irradiation group. H1975 cells were pretreated with Apo-2L under different concentrations of 200 and 228 ng/ml at 24 h before irradiation with doses of 1,1.5,2,2.5,3,3.5 and 4 Gy. The apoptosis rates of all groups were analyzed by flow cytometry 24 h post-irradiation. The inhibition rates of cell proliferation were measured by the MTT assay. Results MTT assay showed that the Apo-2L treatment significantly inhibited cell proliferation(χ2=136.17,P<0.05). The apoptosis rates of the four groups were different significantly, and the apoptosis rate of radiation combined with drug group was significantly higher than the other three groups(χ2=78.02,P<0.05). Conclusions The Apo-2L could not only inhibit the proliferation but also promote radiation-induced apoptosis of adenocarcinoma H1975 cells.
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