81P - Radiation resistance induced immunity evasion by evoking PD-L1 expression

Date 15 April 2016
Event European Lung Cancer Conference 2016 (ELCC) 2016
Session Poster lunch
Topics Immunotherapy
Thoracic malignancies
Translational Research
Surgical oncology
Basic Principles in the Management and Treatment (of cancer)
Radiation oncology
Presenter Xiaomei Gong
Citation Journal of Thoracic Oncology (2016) 11 (supplement 4): S57-S166. S1556-0864(16)X0004-4
Authors X. Gong1, X. Li2, C. Zhou2
  • 1Radiation, Shanghai Pulmonary Hospital, Tongji University, 200433 - Shanghai/CN
  • 2Oncology, Shanghai Pulmonary Hospital, Tongji University, 200433 - Shanghai/CN



Patients with local advanced non-small-cell lung cancer (NSCLC) frequently receive prolonged treatment with chemotherapy and/or fractionated radiotherapy (RT). Unfortunately, local relapses often occur following RT. The PD1/PD-L1 axis is involved in the maintenance of peripheral tolerance through inhibition of T cell function. In our study, we would characterize PD-L1 expression in NSCLC cell lines, and explore the relationship between immunology escaping and tumor proliferation and apoptosis with receiving radiotherapy.


Evaluating the PD-L1 protein and CD8+ T cells with immunohistochemistry in tumor tissue from NSCLC patients. In vitro assay, to study the difference between A549 and radiation resistance A549 cell line by flow cytometry and westernbloting. To analysis PI3K/Akt and stat3 proliferation pathway and Bcl2 family apoptosis signaling pathway in A549 radiation resistance cell by westernbloting. Small interfering RNA (siRNA) was used to A549 radiation resistance cell, and then to observe the difference in PI3K/Akt and stat3 pathway. As for in vivo study, immunohistochemistry was used to detect the relationship between the expression of PD-L1 and NF-KB protein in control group, anti-PD-L1 group, radiation group and radiation plus anti-PD-L1 group.


Patients whose tumor expression the higher PD-L1 protein, who had the more radiation resistance and had less CD8+ T cell around tumor microenvironment. A549 radiation resistance cell had activation in PI3K/Akt and stat3 pathway and its NF-KB protein would be up regulation. We observed the activation of the anti-apoptosis protein bcl2 and the inhibition of the pro-apoptosis protein bim in A549 radiation resistance cell. After siRNA interfering to this cell, its PD-L1 protein decreased. A549 radiation resistance cell came to be apoptosic. While its pAkt, pstat3 and NF-KB didn't change.


RT would induce radiation resistance by evoking the PD-L1 protein. When the lung cancer cell express PD-L1 protein more, the tumor would escape from killing of the CD8+ T cell. NF-KB protein is a key to up-regulation PD-L1. When PD-L1 upregulation, lung cancer would be apoptosis less and immunity escaping. SiRNA interfering PD-L1 can eliminate the radiation resistance of the A549 cell line.

Clinical trial identification

This is a research study, not a clinical trial.

Legal entity responsible for the study

Shanghai pulmonary hospital


Supported by the Youth Project of Science and Technology of Shanghai (12ZR1448100); Scientific Research Foundation of Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China; the scientific Research Foundation of Shanghai Municipal Commission of Health and Family Planning.


All authors have declared no conflicts of interest.