Abstract

Simple SummaryThe molecular progression of prostate cancer is complex and elusive. Biological research relies heavily on in vitro and in vivo models that can be used to examine gene functions and responses to the external agents in laboratory and preclinical settings. Over the years, several models have been developed and found to be very helpful in understanding the biology of prostate cancer. Here we describe these models in the context of available information on the cellular and molecular progression of prostate cancer to suggest their potential utility in basic and preclinical prostate cancer research. The information discussed herein should serve as a hands-on resource for scholars engaged in prostate cancer research or to those who are making a transition to explore the complex biology of prostate cancer.We have witnessed noteworthy progress in our understanding of prostate cancer over the past decades. This basic knowledge has been translated into efficient diagnostic and treatment approaches leading to the improvement in patient survival. However, the molecular pathogenesis of prostate cancer appears to be complex, and histological findings often do not provide an accurate assessment of disease aggressiveness and future course. Moreover, we also witness tremendous racial disparity in prostate cancer incidence and clinical outcomes necessitating a deeper understanding of molecular and mechanistic bases of prostate cancer. Biological research heavily relies on model systems that can be easily manipulated and tested under a controlled experimental environment. Over the years, several cancer cell lines have been developed representing diverse molecular subtypes of prostate cancer. In addition, several animal models have been developed to demonstrate the etiological molecular basis of the prostate cancer. In recent years, patient-derived xenograft and 3-D culture models have also been created and utilized in preclinical research. This review is an attempt to succinctly discuss existing information on the cellular and molecular progression of prostate cancer. We also discuss available model systems and their tested and potential utility in basic and preclinical prostate cancer research.

Highlights

  • Prostate cancer (PCa) is the most commonly diagnosed malignancy and the second leading cause of cancer-related death in men in the United States

  • Low-grade and high-grade prostate intraepithelial neoplasia (PIN) lesions develop from normal prostate epithelium through the loss of phosphatase and the tensin homolog (PTEN), NK3 Homeobox 1 (NKX3.1), overexpression of MYC proto-oncogene, B-cell lymphoma 2 (BCL-2), and the glutathione S-transferase pi 1 gene (GSTP1), accompanied with Speckle Type

  • In the past years, understanding of PCa pathobiology paired with mechanistic studies has remarkably advanced the field of PCa research

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Summary

Introduction

Prostate cancer (PCa) is the most commonly diagnosed malignancy and the second leading cause of cancer-related death in men in the United States. These efforts have resulted in novel therapies that are currently in clinics, while researchers continue to gather more insights to address new hurdles and failures faced in clinical settings These advances have been possible through the development of several in vitro and in vivo research models, while new models continue to be developed to address the genetic and biological complexities associated with the PCa. In this review, we discuss the cellular and molecular progression of PCa as well as the available in vitro and in vivo models for PCa research. We believe that the information presented will be helpful to the researchers, especially those who are new to the field, in understanding the molecular pathobiology of PCa and guide them in choosing the correct model(s) for their laboratory and preclinical research

Cellular and Molecular Progression of Prostate Cancer
Prostate Cancer Research Models
Non-Cancerous Prostate Epithelial Cell Lines
Prostate Cancer Cell Lines
Genetically Engineered Mouse Models of Prostate Cancer
Pten Deficient Mice
Patient Tumor-Derived Models
Rat Models
Zebrafish Model
Findings
Conclusions and Future Outlook
Full Text
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