Autophagy and prostate cancer therapeutics

Hsing Jien Kung, Chun Changou, Hao G. Nguyen, Joy C. Yang, Christopher P. Evans, Richard J. Bold, Frank Chuang

Research output: Chapter in Book/Report/Conference proceedingChapter

10 Citations (Scopus)


Autophagy or self-eating is an evolutionarily conserved process whereby cells, in response to stress conditions, use lysosomal-mediated degradation of longlived proteins and retired organelles to regenerate energy. It protects cells from harsh conditions and prolongs cell survival. Cancer therapeutics induce a variety of stresses in tumor cells including nutritional starvation, DNA damage, ER stress, and ROS generation. Not surprisingly, the great majority of cancer therapeutics also induce autophagy. As such, autophagy becomes an inseparable part of cancer therapy and its modulation, and thus deserve attention. In this review, we discuss the current prostate cancer therapies, the cell biology and detection method of autophagy, the relationship of autophagy to apoptosis and necroptosis, and autophagy modulation in experimental prostate cancer therapies. Finally, we provide a comprehensive summary of the autophagy characteristics (induction and function) of experimental and clinically tested prostate cancer treatments, as well as current clinical trials involving autophagy modulators.

Original languageEnglish
Title of host publicationProstate Cancer
Subtitle of host publicationBiochemistry, Molecular Biology and Genetics
PublisherSpringer New York
Number of pages22
ISBN (Electronic)9781461468288
ISBN (Print)9781461468271
Publication statusPublished - Jan 1 2013
Externally publishedYes

ASJC Scopus subject areas

  • General Medicine


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