The Prospect of Identifying Resistance Mechanisms for Castrate-Resistant Prostate Cancer Using Circulating Tumor Cells: Is Epithelial-to-Mesenchymal Transition a Key Player?

Prostate cancer (PCa) is initially driven by excessive androgen receptor (AR) signaling with androgen deprivation therapy (ADT) being a major therapeutic approach to its treatment. However, the development of drug resistance is a significant limitation on the effectiveness of both first-line and mor...

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Bibliographic Details
Published in:Prostate cancer 2020, Vol.2020 (2020), p.1-16
Main Authors: de Souza, Paul, Nimir, Mohammed, Lock, John, Becker, Therese M., Scott, Kieran F., Khan, Tanzila, Ma, Yafeng
Format: Article
Language:English
Subjects:
Analysis
Androgens
Apoptosis
B cells
Biomarkers
Cancer therapies
Cell adhesion & migration
Cell growth
Development and progression
Drug resistance
Gene expression
Health aspects
Hypoxia
Kinases
Liver cancer
Metastasis
Mortality
Patients
Prostate cancer
Review
Stem cells
Transcription factors
Tumors
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Summary:Prostate cancer (PCa) is initially driven by excessive androgen receptor (AR) signaling with androgen deprivation therapy (ADT) being a major therapeutic approach to its treatment. However, the development of drug resistance is a significant limitation on the effectiveness of both first-line and more recently developed second-line ADTs. There is a need then to study AR signaling within the context of other oncogenic signaling pathways that likely mediate this resistance. This review focuses on interactions between AR signaling, the well-known phosphatidylinositol-3-kinase/AKT pathway, and an emerging mediator of these pathways, the Hippo/YAP1 axis in metastatic castrate-resistant PCa, and their involvement in the regulation of epithelial-mesenchymal transition (EMT), a feature of disease progression and ADT resistance. Analysis of these pathways in circulating tumor cells (CTCs) may provide an opportunity to evaluate their utility as biomarkers and address their importance in the development of resistance to current ADT with potential to guide future therapies.
ISSN:2090-3111
2090-312X
DOI:10.1155/2020/7938280