| Chu Xiaofei,Xue Xiaolei,Zhao Shuyi,Zheng Qisheng,Fan Saijun.Hepatitis B X-interacting protein (HBXIP) inhibits autophagy induced by ionizing radiation in breast cancer cells[J].Chinese Journal of Radiological Medicine and Protection,2016,36(11):801-805 |
| Hepatitis B X-interacting protein (HBXIP) inhibits autophagy induced by ionizing radiation in breast cancer cells |
| Received:May 13, 2016 |
| DOI：10.3760/cma.j.issn.0254-5098.2016.11.001 |
| KeyWords:Breast cancer Hepatitis B X-interacting protein STAT3 Autophagy |
| FundProject:国家自然科学基金（81502664，81402541，81172127）；科技部科研院所技术发展研究专项（2014EG150134）；天津科技支撑计划项目（14ZCZDSY00001） |
| Author Name | Affiliation | E-mail | | Chu Xiaofei | Tianjin Key Laboratory of Radiation Medicine and Molecular Nuclear Medicine, Institute of Radiation Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin 300192, China | | | Xue Xiaolei | Tianjin Key Laboratory of Radiation Medicine and Molecular Nuclear Medicine, Institute of Radiation Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin 300192, China | | | Zhao Shuyi | Tianjin Key Laboratory of Radiation Medicine and Molecular Nuclear Medicine, Institute of Radiation Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin 300192, China | | | Zheng Qisheng | Tianjin Key Laboratory of Radiation Medicine and Molecular Nuclear Medicine, Institute of Radiation Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin 300192, China | | | Fan Saijun | Tianjin Key Laboratory of Radiation Medicine and Molecular Nuclear Medicine, Institute of Radiation Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin 300192, China | fansaijun@irm-cams.ac.cn |
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| Abstract:: |
| Objective To explore the effect of HBXIP on the autophagy induced by ionizing radiation in breast cancer cells. Methods Experiments included control group, HBXIP transfected group, si-HBXIP transfected group, HBXIP and si-STAT3 co-transfected group. Each group was given 4 Gy γ-ray irradiation exposure. Autophagosomes and autolysosomes (AVOs) were quantified by flow cytometry, and the expressions of LC3, HBXIP, STAT3 and STAT3(Y705) phosphorylation proteins were detected by Western blot assay at 0, 24, 48, 72 h post-irradiation. Results Overexpression of HBXIP significantly reduced the increases of AVOs formation(24 h:t=3.67, P<0.05; 48 h:t=9.74, P<0.01; 72 h:t=10.15, P<0.01) and LC3-II protein expression, while si-RNA-mediated depletion of HBXIP expression markedly improved AVOs formation(24 h:t=3.5, P<0.05; 48 h:t=4.15, P<0.05; 72 h:t=12.12, P<0.01) and LC3-II protein expression in irradiated breast cancer cells. In addition, an increased phosphorylation level of STAT3 protein at Y705 in the cells overexpressed HBXIP, and a decreased phosphorylation of STAT3 protein in the cells with silencing HBXIP were observed following irradiation. Meanwhile, STAT3 siRNA inhibited HBXIP functions in regulation of AVOs formation(24 h:t=5.57, P<0.05; 48 h:t=13.65, P<0.01; 72 h:t=12.47, P<0.01) and LC3-II expression in irradiated cells. Conclusions HBXIP inhibits autophagy caused by radiation in breast cancer cells by mediating STAT3 phosphorylation. |
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