Dual role of autophagy on docetaxel-sensitivity in prostate cancer cells.

Cell Death & Disease
Riccardo CristofaniRoberta Manuela Moretti

Abstract

Prostate cancer (PC) is one of the leading causes of death in males. Available treatments often lead to the appearance of chemoresistant foci and metastases, with mechanisms still partially unknown. Within tumour mass, autophagy may promote cell survival by enhancing cancer cells tolerability to different cell stresses, like hypoxia, starvation or those triggered by chemotherapic agents. Because of its connection with the apoptotic pathways, autophagy has been differentially implicated, either as prodeath or prosurvival factor, in the appearance of more aggressive tumours. Here, in three PC cells (LNCaP, PC3, and DU145), we tested how different autophagy inducers modulate docetaxel-induced apoptosis. We selected the mTOR-independent disaccharide trehalose and the mTOR-dependent macrolide lactone rapamycin autophagy inducers. In castration-resistant PC (CRPC) PC3 cells, trehalose specifically prevented intrinsic apoptosis in docetaxel-treated cells. Trehalose reduced the release of cytochrome c triggered by docetaxel and the formation of aberrant mitochondria, possibly by enhancing the turnover of damaged mitochondria via autophagy (mitophagy). In fact, trehalose increased LC3 and p62 expression, LC3-II and p62 (p62 bodies) accu...Continue Reading

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May 28, 2019·Cells·Monica Vara-PerezPatrizia Agostinis
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Methods Mentioned

BETA
nuclear translocation
electrophoresis
fluorescence microscopy
confocal microscopy
flow cytometry
ubiquitination
transfection
PCR
protein assay

Software Mentioned

Primer
PRISM
GraphPad
ImageJ
Aim
Image Lab

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