Publication in refereed journal
香港中文大学研究人员 ( 现职)
| 于君教授 (内科及药物治疗学系) |
| 陈家亮教授 (内科及药物治疗学系) |
| 李中华先生 (内科及药物治疗学系) |
| 曹之宪教授 (生物医学学院) |
| 胡嘉麒教授 (麻醉及深切治疗学系) |
全文
| 数位物件识别号 (DOI) http://dx.doi.org/10.1038/onc.2011.295 |
引用次数
Web of Sciencehttp://aims.cuhk.edu.hk/converis/portal/Publication/105WOS source URL
其它资讯
摘要Autophagy, hallmarked by the formation of double-membrane bound organelles known as autophagosomes, is a lysosome-dependent pathway for protein degradation. The role of autophagy in carcinogenesis is context dependent. As a tumor-suppressing mechanism in early-stage carcinogenesis, autophagy inhibits inflammation and promotes genomic stability. Moreover, disruption of autophagy-related genes accelerates tumorigenesis in animals. However, autophagy may also act as a pro-survival mechanism to protect cancer cells from various forms of cellular stress. In cancer therapy, adaptive autophagy in cancer cells sustains tumor growth and survival in face of the toxicity of cancer therapy. To this end, inhibition of autophagy may sensitize cancer cells to chemotherapeutic agents and ionizing radiation. Nevertheless, in certain circumstances, autophagy mediates the therapeutic effects of some anticancer agents. Data from recent studies are beginning to unveil the apparently paradoxical nature of autophagy as a cell-fate decision machinery. Taken together, modulation of autophagy is a novel approach for enhancing the efficacy of existing cancer therapy, but its Janus-faced nature may complicate the clinical development of autophagy modulators as anticancer therapeutics. Oncogene (2012) 31, 939-953; doi:10.1038/onc.2011.295; published online 18 July 2011
着者Wu WKK, Coffelt SB, Cho CH, Wang XJ, Lee CW, Chan FKL, Yu J, Sung JJY
期刊名称Oncogene
出版年份2012
月份2
日期1
卷号31
期次8
出版社Nature Publishing Group: Open Access Hybrid Model Option B
页次939 - 953
国际标準期刊号0950-9232
电子国际标準期刊号1476-5594
语言英式英语
关键词autophagy; cell death; cell survival
Web of Science 学科类别Biochemistry & Molecular Biology; BIOCHEMISTRY & MOLECULAR BIOLOGY; Cell Biology; CELL BIOLOGY; Genetics & Heredity; GENETICS & HEREDITY; Oncology; ONCOLOGY
