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 language||English (US)|
|Title of host publication||Prostate Cancer|
|Subtitle of host publication||Biochemistry, Molecular Biology and Genetics|
|Publisher||Springer New York|
|Number of pages||22|
|State||Published - Jan 1 2013|
ASJC Scopus subject areas