Published June 2016 | Version v1
Journal article

The effect of apoptosis-2 ligand on irradiation-induced apoptosis in lung adenocarcinima H1975 cells resistant to EGFR-TKI

  • 1. Department of Oncology, Affiliated Hospital of Qingdao University, Qingdao (China)
  • 2. Department of Oncology, Qingdao Central Hospital, Qingdao (China)
  • 3. Department of Oncology, Linyi People's Hospital, Linyi (China)

Description

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. (authors)

Additional details

Publishing Information

Journal Title
Chinese Journal of Radiological Medicine and Protection
Journal Volume
36
Journal Issue
6
Journal Page Range
p. 424-429
ISSN
0254-5098

Optional Information

Notes
1 fig., 3 tabs., 22 refs.; http://dx.doi.org/10.3760/cma.j.issn.0254-5098.2016.06.005