A comparison of the biological effects of 125I seeds continuous low-dose-rate radiation and 60Co high-dose-rate gamma radiation on non-small cell lung cancer cells.
OBJECTIVE
To compare the biological effects of 125I seeds continuous low-dose-rate (CLDR) radiation and 60Co γ-ray high-dose-rate (HDR) radiation on non-small cell lung cancer (NSCLC) cells.


METHODS
A549, H1299 and BEAS-2B cells were exposed to 125I seeds CLDR radiation or 60Co γ-ray HDR radiation. The survival fraction was determined using a colony-forming assay. The cell cycle progression and apoptosis were detected by flow cytometry (FCM). The expression of the apoptosis-related proteins caspase-3, cleaved-caspase-3, PARP, cleaved-PARP, BAX and Bcl-2 were detected by western blot assay.


RESULTS
After irradiation with 125I seeds CLDR radiation, there was a lower survival fraction, more pronounced cell cycle arrest (G1 arrest and G2/M arrest in A549 and H1299 cells, respectively) and a higher apoptotic ratio for A549 and H1299 cells than after 60Co γ-ray HDR radiation. Moreover, western blot assays revealed that 125I seeds CLDR radiation remarkably up-regulated the expression of Bax, cleaved-caspase-3 and cleaved-PARP proteins and down-regulated the expression of Bcl-2 proteins in A549 and H1299 cells compared with 60Co γ-ray HDR radiation. However, there was little change in the apoptotic ratio and expression of apoptosis-related proteins in normal BEAS-2B cells receiving the same treatment.


CONCLUSIONS
125I seeds CLDR radiation led to remarkable growth inhibition of A549 and H1299 cells compared with 60Co HDR γ-ray radiation; A549 cells were the most sensitive to radiation, followed by H1299 cells. In contrast, normal BEAS-2B cells were relatively radio-resistant. The imbalance of the Bcl-2/Bax ratio and the activation of caspase-3 and PARP proteins might play a key role in the anti-proliferative effects induced by 125I seeds CLDR radiation, although other possibilities have not been excluded and will be investigated in future studies.
Institution of Molecular Imaging, Southeast University, Nanjing, China; Department of Interventional Radiology, The Third Affiliated Hospital of the Medical College Shihezi University, Xinjiang, China; Department of Radiology, Ruijin Hospital Luwan Branch, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Zhongmin
Z
Wang
Department of Radiology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Department of Interventional Radiology, Shanghai St. Luke's Hospital, Shanghai, China.
Zhenzhen
Z
Zhao
Department of Radiology, Ruijin Hospital Luwan Branch, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jian
J
Lu
Department of Radiology, Ruijin Hospital Luwan Branch, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Zhijin
Z
Chen
Department of Interventional Radiology, Shanghai St. Luke's Hospital, Shanghai, China.
Aiwu
A
Mao
Institution of Molecular Imaging, Southeast University, Nanjing, China.
Gaojun
G
Teng
Department of Radiobiology, School of Radiological Medicine and Protection, Soochow University, Suzhou, China.
Fenju
F
Liu
D017209:Apoptosis / Q000528:radiation effects; D002289:Carcinoma, Non-Small-Cell Lung / Q000235:genetics / Q000473:pathology / Q000532:radiotherapy*; D002453:Cell Cycle / Q000528:radiation effects; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000528:radiation effects*; D003037:Cobalt Radioisotopes / Q000009:adverse effects / Q000627:therapeutic use; D004307:Dose-Response Relationship, Radiation; D005434:Flow Cytometry; D005720:Gamma Rays / Q000009:adverse effects / Q000627:therapeutic use*; D015972:Gene Expression Regulation, Neoplastic / Q000528:radiation effects; D006801:Humans; D007457:Iodine Radioisotopes / Q000009:adverse effects / Q000627:therapeutic use; D009363:Neoplasm Proteins / Q000096:biosynthesis* / Q000235:genetics
D003037:Cobalt Radioisotopes; D007457:Iodine Radioisotopes; D009363:Neoplasm Proteins