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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
TGFBR3 loss and consequences in prostate cancer
Nima Sharifi1, Elaine M Hurt, Brian T Kawasaki
1Cancer Stem Cell Section, Laboratory of Cancer Prevention, National Cancer Institute at Frederick, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, Maryland 21702, USA. nima.sharifi@nih.gov
The Prostate
|December 29, 2006
Summary
Transforming growth factor-beta receptor 3 (TGFBR3) downregulation is common in prostate cancer. Its loss promotes cancer stem cell markers and genes involved in tumor growth, indicating its role in tumorigenesis.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Transforming growth factor-beta (TGF-beta) resistance is crucial in cancer development.
- Mechanisms of TGF-beta resistance in prostate cancer remain largely unknown.
Purpose of the Study:
- To investigate the role of TGF-beta pathway components in prostate cancer.
- To elucidate the function of TGFBR3 in prostate tumorigenesis.
Main Methods:
- Systematic analysis of TGF-beta pathway components using meta-analysis of seven microarray studies.
- Evaluation of TGFBR3 expression in prostate cell lines.
- Functional analysis of TGFBR3 knockdown in prostate epithelial cells.
Main Results:
- TGFBR3 was the most frequently downregulated TGF-beta component in localized prostate cancer.
- TGFBR3 knockdown induced focus formation and increased CD133 expression, a prostate cancer stem cell marker.
- Microarray analysis revealed 101 genes regulated by TGFBR3, including those involved in prostate mass and vasculature.
Conclusions:
- Downregulation of TGFBR3 is a significant event in prostate cancer progression.
- TGFBR3 plays a critical role in regulating genes associated with tumor growth and development.
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