Related Experiment Video

Updated: Apr 13, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
07:25

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer

Published on: March 6, 2018

14.0K

Regulation of tumor cell plasticity by the androgen receptor in prostate cancer

Jennifer L Bishop1, Alastair Davies1, Kirsi Ketola1

  • 1The Vancouver Prostate Centre2660 Oak Street, Vancouver, British Columbia, Canada V6H-3Z6Department of Urologic SciencesUniversity of British Columbia, Vancouver, British Columbia, Canada The Vancouver Prostate Centre2660 Oak Street, Vancouver, British Columbia, Canada V6H-3Z6Department of Urologic SciencesUniversity of British Columbia, Vancouver, British Columbia, Canada.

Endocrine-Related Cancer
|May 3, 2015
PubMed

Insights

Prostate cancer (PCa) progression is driven by cellular plasticity, where cells adapt to androgen-deprivation therapies. Targeting this adaptability offers new strategies to combat aggressive PCa.

Area of Science:

  • Oncology
  • Cancer Biology
  • Endocrinology

Background:

  • Prostate cancer (PCa) is a leading cause of cancer-related deaths in men.
  • Hormonal therapies targeting androgen receptor (AR) signaling are standard PCa treatment.
  • AR signaling is crucial for PCa development and progression.

Purpose of the Study:

  • To review the cellular plasticity induced by androgen deprivation in prostate cancer.
  • To examine how AR signaling regulates cancer stem-like cells, epithelial-mesenchymal/myeloid plasticity, and neuroendocrine transdifferentiation.
  • To explore novel therapeutic strategies targeting therapy-induced cellular plasticity in aggressive PCa.

Main Methods:

  • Review of existing scientific literature on prostate cancer cellular plasticity.
  • Analysis of AR's role in regulating adaptive cell phenotypes under androgen deprivation.
  • Examination of therapeutic approaches targeting AR-regulated cellular plasticity.

Main Results:

  • Androgen-deprivation therapies induce heterogeneous cell populations in PCa.
  • Emergence of cancer stem-like cells, epithelial-mesenchymal/myeloid plasticity, and neuroendocrine transdifferentiation are key adaptive phenotypes.
  • These phenotypes are regulated by the androgen receptor (AR) and associated with aggressive disease.

Conclusions:

  • Cellular plasticity is a critical mechanism driving treatment resistance and progression in advanced prostate cancer.
  • Targeting AR-mediated cellular plasticity presents a promising therapeutic avenue.
  • Developing novel strategies to counteract these adaptive phenotypes could improve outcomes for patients with aggressive PCa.
Keywords:
androgen receptorendocrine therapy resistanceprostate

More Related Videos

Prostate Organoid Cultures as Tools to Translate Genotypes and Mutational Profiles to Pharmacological Responses08:36

Prostate Organoid Cultures as Tools to Translate Genotypes and Mutational Profiles to Pharmacological Responses

Published on: October 24, 2019

11.8K
Evaluating the Differentiation Capacity of Mouse Prostate Epithelial Cells Using Organoid Culture10:38

Evaluating the Differentiation Capacity of Mouse Prostate Epithelial Cells Using Organoid Culture

Published on: November 22, 2019

9.7K

Related Concept Videos

mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
5.1K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

1.7K
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
5.4K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
8.5K
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
39.2K
Epigenetic Regulation01:37

Epigenetic Regulation

Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
4.3K