Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/95829
標題: Cytolethal Distending Toxin Enhances Radiosensitivity in Prostate Cancer Cells by Regulating Autophagy
作者: Lin, Hwai-Jeng
Liu, Hsin-Ho
Lin, Chia-Der
Kao, Min-Chuan
Chen, Yu-An
Chiang-Ni, Chuan
Jiang, Zhi-Pei
Huang, Mei-Zi
Lin, Chun-Jung
Lo, U-Ging
Lin, Li-Chiung
Lai, Cheng-Kuo
林赫
Lin, Ho
Hsieh, Jer-Tsong
Chiu, Cheng-Hsun
Lai, Chih-Ho
關鍵字: Campylobacter jejuni
autophagy
cell cycle
cytolethal distending toxin
radioresistance
Animals
Apoptosis
Autophagosomes
Autophagy
Bacterial Toxins
Campylobacter jejuni
Cell Cycle
Cell Cycle Checkpoints
Cell Line
Drug Therapy, Combination
HMGB1 Protein
Humans
Male
Mice
Prostate
Prostatic Neoplasms
Radiation Tolerance
出版社: FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
摘要: Cytolethal distending toxin (CDT) produced by Campylobacter jejuni contains three subunits: CdtA, CdtB, and CdtC. Among these three toxin subunits, CdtB is the toxic moiety of CDT with DNase I activity, resulting in DNA double-strand breaks (DSB) and, consequently, cell cycle arrest at the G2/M stage and apoptosis. Radiation therapy is an effective modality for the treatment of localized prostate cancer (PCa). However, patients often develop radioresistance. Owing to its particular biochemical properties, we previously employed CdtB as a therapeutic agent for sensitizing radioresistant PCa cells to ionizing radiation (IR). In this study, we further demonstrated that CDT suppresses the IR-induced autophagy pathway in PCa cells by attenuating c-Myc expression and therefore sensitizes PCa cells to radiation. We further showed that CDT prevents the formation of autophagosomes via decreased high-mobility group box 1 (HMGB1) expression and the inhibition of acidic vesicular organelle (AVO) formation, which are associated with enhanced radiosensitivity in PCa cells. The results of this study reveal the detailed mechanism of CDT for the treatment of radioresistant PCa.
URI: http://hdl.handle.net/11455/95829
文章連結: https://www.ncbi.nlm.nih.gov/pubmed/28642840
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