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Updated: Jun 5, 2026

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

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

Published on: November 22, 2019

Dysregulated Cell Signaling Pathways in Prostate Tumoral Plasticity-Checkpoints.

Elena Matei¹, Ionuț Ciprian Iorga^2,3, Mariana Deacu^2,4

¹Center for Research and Development of the Morphological and Genetic Studies of Malignant Pathology, "Ovidius" University of Constanta, 145 Tomis Blvd., Constanta, Romania.

Oncology Research

|June 4, 2026

Summary

This summary is machine-generated.

Cell cycle S-phase predicts prostate cancer outcomes. Low S-phase indicates better survival in benign prostatic hyperplasia, while high S-phase suggests poorer survival in prostate cancer, impacting treatment strategies.

Keywords:

DNA damage Epithelial-mesenchymal transition (EMT)autophagy microenvironment necrosis-apoptosis continuum transcription factor p53

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Isolation of Cancer Stem Cells From Human Prostate Cancer Samples

Isolation of Cancer Stem Cells From Human Prostate Cancer Samples

Published on: March 14, 2014

Area of Science:

Oncology
Cell Biology
Cancer Research

Background:

Deregulated cellular plasticity drives cancer initiation, progression, metastasis, and therapy resistance.
Epithelial-mesenchymal transition (EMT) is a key process in tumor cell plasticity, characterized by significant variability and heterogeneity.
Understanding the checkpoints governing EMT heterogeneity is crucial for developing effective cancer therapies.

Purpose of the Study:

To identify novel checkpoints regulating epithelial-mesenchymal transition (EMT) variability in prostate cancer.
To analyze intrinsic and extrinsic factors contributing to prostate EMT heterogeneity.
To establish prognostic biomarkers for benign prostatic hyperplasia (BPH) and prostate cancer (PCa) based on cell cycle dynamics.

Main Methods:

Cell cycle phases analyzed using propidium iodide (PI) staining.
Apoptosis assessed via caspase-3/7 activity (DEVD-MR/PI staining).
Autophagy and nuclear shrinkage evaluated using Hoechst/acridine orange staining.
Immune surveillance evasion studied using CD42b-PE staining.
Oxidative stress quantified by reactive oxygen species (ROS) count via flow cytometry.
Microenvironment adaptation analyzed by immunohistochemistry (IHC).

Main Results:

In BPH, a low S-proliferative phase (<7%) is an independent predictor of favorable patient survival, linked to dysregulated EMT signaling pathways.
In PCa, a high S-proliferative phase (>12%) is associated with unfavorable survival, indicating an aggressive phenotype and EMT heterogeneity.
High S-phase in PCa correlates with late apoptosis, necrosis, autophagy, immune evasion, cell cycle arrest, and oxidative stress.

Conclusions:

Cell cycle S-phase categories (low and high) are critical checkpoints in EMT heterogeneity.
Dysregulated apoptosis via the caspase-3/7 pathway is also a key factor in EMT heterogeneity.
These cell cycle and apoptosis markers serve as independent or dependent predictors for BPH and PCa patient survival, aiding personalized therapy development.