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CRISP3 expression drives prostate cancer invasion and progression
Marianna Volpert1, Luc Furic1,2,3,4, Jinghua Hu1,5
1Department of Anatomy and Developmental Biology, Monash University, Clayton, Victoria, Australia.
Endocrine-Related Cancer
|May 2, 2020
Summary
Cysteine-rich secretory protein 3 (CRISP3) drives prostate cancer progression by enhancing cell migration and invasion. Targeting CRISP3 offers a potential therapeutic strategy for prostate cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Prostate cancer progression involves increased cell migration and invasion.
- Cysteine-rich secretory protein 3 (CRISP3) is significantly upregulated in prostate cancer.
Purpose of the Study:
- To investigate the role of CRISP3 in prostate cancer progression.
- To identify CRISP3 as a potential therapeutic target.
Main Methods:
- Utilized a genetically engineered mouse model of prostate cancer.
- Employed human and mouse prostate cancer cell lines.
- Performed mass spectrometry to analyze protein abundance changes.
Main Results:
- CRISP3 production accelerated prostate cancer progression in vivo.
- Exposure to CRISP3 enhanced prostate cancer cell motility and invasion.
- CRISP3 altered the abundance of cell-cell adhesion proteins, including LASP1 and TJP1.
Conclusions:
- CRISP3 acts as a pro-tumorigenic factor in prostate cancer.
- CRISP3 is a validated therapeutic target for prostate cancer intervention.
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