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Identification, Histological Characterization, and Dissection of Mouse Prostate Lobes for In Vitro 3D Spheroid Culture Models
Published on: September 18, 2018
A mouse prostate cancer model induced by Hedgehog overexpression
Bo-Yie Chen1, David Pei-Cheng Lin, Jer-Yuh Liu
1Institute of Biochemistry and Biotechnology, Chung Shan Medical University, Taichung, Taiwan.
Journal of Biomedical Science
|December 24, 2005
Summary
Hedgehog protein overexpression can initiate prostate cancer (CaP) development in mice. This study establishes a new mouse model for testing therapies targeting the Hedgehog signaling pathway in prostate cancer.
Area of Science:
- Oncology
- Molecular Biology
- Developmental Biology
Background:
- Hedgehog signaling is crucial for embryonic development.
- Abnormal Hedgehog activation is linked to tumorigenesis in epithelial-mesenchymal interaction sites.
- Hedgehog signaling is observed in advanced prostate cancer but its role in initiation is unknown.
Purpose of the Study:
- To investigate if Hedgehog overexpression can initiate prostate tumorigenesis.
- To establish a mouse model for prostate cancer induced by Hedgehog overexpression.
Main Methods:
- Intra-prostate injection and electroporation of a Hedgehog-expressing vector in mice.
- Immunohistochemistry and Western blot to confirm Hedgehog overexpression.
- Histopathological analysis to assess tumorigenic phenotypes.
Main Results:
- Hedgehog overexpression induced prostatic intraepithelial neoplasia and prostatic cancer (CaP) phenotypes within 30 days.
- Tumorigenic phenotypes included loss of basal cell marker p63, epithelial cell mix-up in stroma, and absence of alpha-SMA.
- Comparable Hedgehog overexpression was detected in human CaP specimens.
Conclusions:
- Hedgehog overexpression is sufficient to induce prostate tumorigenesis from a normal state.
- A novel mouse model for Hedgehog-induced prostate cancer has been established.
- This model can be utilized for evaluating novel therapeutic strategies targeting the Hedgehog signaling pathway.
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