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Inhibiting autophagy with chloroquine enhances the anti-tumor effect of high-LET carbon ions via ER stress-related apoptosis

文献类型：期刊论文

作者Zheng, Xiaogang1,2,3,4; Jin, Xiaodong1,2,3; Li, Feifei1,2,3,4; Liu, Xiongxiong1,2,3; Liu, Yan1,2,3,4; Ye, Fei1,2,3; Li, Ping1,2,3; Zhao, Ting1,2,3; Li, Qiang1,2,3
刊名MEDICAL ONCOLOGY
出版日期2017-02-01
卷号34页码:10
关键词High-LET radiation Autophagy Chloroquine ER stress Apoptosis CHOP
ISSN号1357-0560
DOI10.1007/s12032-017-0883-8
英文摘要Energetic carbon ions (CI) offer great advantages over conventional radiations such as X-or c-rays in cancer radiotherapy. High linear energy transfer (LET) CI can induce both endoplasmic reticulum (ER) stress and autophagy in tumor cells under certain circumstances. The molecular connection between ER stress and autophagy in tumor exposed to high-LET radiation and how these two pathways influence the therapeutic effect against tumor remain poorly understood. In this work, we studied the impact of autophagy and apoptosis induced by ER stress following high-LET CI radiation on the radiosensitivity of S180 cells both in vitro and in vivo. In the in vitro experiment, X-rays were also used as a reference radiation. Our results documented that the combination of CI radiation with chloroquine (CQ), a special autophagy inhibitor, produced more pronounced proliferation suppression in S180 cells and xenograft tumors. Co-treatment with CI radiation and CQ could block autophagy through the IRE1/JNK/Beclin-1 axis and enhance apoptotic cell death via the activation of C/EBP homologous protein (CHOP) by the IRE1 pathway rather than PERK in vitro and in vivo. Thus, our study indicates that inhibiting autophagy might be a promising therapeutic strategy in CI radiotherapy via aggravating the ER stress-related apoptosis.
WOS关键词ENDOPLASMIC-RETICULUM STRESS ; RADIATION-INDUCED AUTOPHAGY ; UNFOLDED PROTEIN RESPONSE ; HUMAN GLIOMA-CELLS ; LUNG-CANCER CELLS ; IONIZING-RADIATION ; TUMOR-CELLS ; IEC-6 CELLS ; IN-VITRO ; DEATH
资助项目Key Project of the National Natural Science Foundation of China[U1232207] ; National Key Technology Support Program of the Ministry of Science and Technology of China[2015BAI01B11] ; National Key Research and Development Program of the Ministry of Science and Technology of China[2016YFC0904602] ; National Natural Science Foundation of China[10905080] ; National Natural Science Foundation of China[11075191] ; National Natural Science Foundation of China[11205217]
WOS研究方向Oncology
语种英语
WOS记录号WOS:000393689000011
出版者HUMANA PRESS INC
资助机构Key Project of the National Natural Science Foundation of China ; National Key Technology Support Program of the Ministry of Science and Technology of China ; National Key Research and Development Program of the Ministry of Science and Technology of China ; National Natural Science Foundation of China
源URL[http://119.78.100.186/handle/113462/44331]  
专题中国科学院近代物理研究所
通讯作者Li, Qiang
作者单位1.Chinese Acad Sci, Inst Modern Phys, 509 Nanchang Rd, Lanzhou 730000, Peoples R China
2.Chinese Acad Sci, Key Lab Heavy Ion Radiat Biol & Med, Lanzhou 730000, Peoples R China
3.Key Lab Basic Res Heavy Ion Radiat Applicat Med, Lanzhou 730000, Gansu, Peoples R China
4.Univ Chinese Acad Sci, Beijing 100049, Peoples R China
推荐引用方式
GB/T 7714		 Zheng, Xiaogang,Jin, Xiaodong,Li, Feifei,et al. Inhibiting autophagy with chloroquine enhances the anti-tumor effect of high-LET carbon ions via ER stress-related apoptosis[J]. MEDICAL ONCOLOGY,2017,34:10.
APA Zheng, Xiaogang.,Jin, Xiaodong.,Li, Feifei.,Liu, Xiongxiong.,Liu, Yan.,...&Li, Qiang.(2017).Inhibiting autophagy with chloroquine enhances the anti-tumor effect of high-LET carbon ions via ER stress-related apoptosis.MEDICAL ONCOLOGY,34,10.
MLA Zheng, Xiaogang,et al."Inhibiting autophagy with chloroquine enhances the anti-tumor effect of high-LET carbon ions via ER stress-related apoptosis".MEDICAL ONCOLOGY 34(2017):10.

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来源：近代物理研究所

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