Abstract:
:Although overall mortality rate of prostate cancer (PCa) declines in recent years, castration-resistant prostate cancer (CRPC) remains incurable. Clinical evidence indicates that CRPC recurred from hormonal therapy exhibits neuroendocrine differentiated (NED) phenotypes, which could contribute to therapeutic resistance and poor survival. Understanding the onset of NED could lead us to develop new therapeutic strategies for CRPC. Although PCa is known as a lipid-enriched tumor, its role in CRPC development is not fully understood. In this study, we demonstrated that IL-6 or androgen deprivation therapy (ADT)-induced lipid accumulation is associated with NED phenotypes. IL-6 or ADT can induce NED in PCa cells via peroxisome proliferator-activated receptor γ (PPARγ, a major lipogenic transcription factor) and adipocyte differentiation-related protein (ADRP, a major component of adiposome). In addition, ADRP protein can be detected in exosomes released from these cells and these exosomes are capable of inducing NED of PCa cells in a paracrine fashion. Understanding the role of PPARγ/ADRP in NED could provide new target(s) for CRPC therapy.
journal_name
Cancer Lettjournal_title
Cancer lettersauthors
Lin LC,Gao AC,Lai CH,Hsieh JT,Lin Hdoi
10.1016/j.canlet.2017.01.018subject
Has Abstractpub_date
2017-04-10 00:00:00pages
74-82eissn
0304-3835issn
1872-7980pii
S0304-3835(17)30041-1journal_volume
391pub_type
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