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A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
Published on: March 6, 2018
Mouse prostate cancer cell lines established from primary and postcastration recurrent tumors
Chun-Peng Liao1, Mengmeng Liang, Michael B Cohen
1Department of Pathology, Keck School of Medicine, University of Southern California, Los Angeles, California, USA.
Hormones & Cancer
|July 16, 2010
Summary
New prostate cancer cell lines were developed from a mouse model. These cell lines represent both androgen-dependent (AD-Ca) and androgen-independent (ADI-Ca) prostate cancer phases, aiding research into prostate cancer progression and androgen metabolism.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Prostate cancer progresses through androgen-dependent (AD-Ca) and androgen-independent (ADI-Ca) phases.
- AD-Ca responds to androgen depletion, while ADI-Ca does not.
- Understanding the molecular differences between these phases is crucial for effective treatment.
Purpose of the Study:
- To generate and characterize novel cell lines modeling both AD-Ca and ADI-Ca.
- To investigate the role of androgen receptor (AR) expression and signaling in different prostate cancer phases.
- To establish preclinical models for studying prostate cancer heterogeneity and therapeutic resistance.
Main Methods:
- Generation of four cell lines (two AD-Ca, two ADI-Ca) from a conditional Pten deletion mouse model.
- Characterization of cell lines for Pten gene deletion, androgen receptor (AR) expression, and epithelial-mesenchymal transition (EMT) markers.
- Inoculation of cell lines into NOD.SCID mice to assess tumor formation and histopathology.
- Analysis of tumor types, including adenocarcinomas and sarcomatoid carcinomas, and their association with cell line origin and host sex.
Main Results:
- Developed AD-Ca (E series) and ADI-Ca (cE series) cell lines with similar AR expression but distinct growth characteristics under androgen deprivation.
- ADI-Ca cell lines showed increased AR transcription in androgen-deprived conditions, unlike AD-Ca cell lines.
- E series cells exhibited markers of EMT (vimentin, Twist, Slug), while cE series cells expressed epithelial markers (CK8, CK14, CK18, E-cadherin).
- Tumorigenicity was confirmed in mice, with cE series forming adenocarcinomas and E series forming sarcomatoid carcinomas.
Conclusions:
- The generated cell lines provide valuable models for studying prostate cancer progression from AD-Ca to ADI-Ca.
- Differences in AR regulation and EMT markers correlate with distinct tumor phenotypes.
- These models will facilitate research into androgen metabolism and therapeutic strategies for advanced prostate cancer.
