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Regulation of prostasin expression and function in the prostate
Li-Mei Chen1, Xiaochun Zhang, Karl X Chai
1Department of Molecular Biology and Microbiology, University of Central Florida, Orlando, Florida 32816, USA.
The Prostate
|March 3, 2004
Summary
Prostate cancer involves reduced prostasin, an invasion suppressor. Researchers identified a prostasin-binding protein (PN-1) that inhibits prostasin activity, revealing environmental regulation of prostasin in prostate cancer.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Prostasin, an invasion suppressor, is downregulated in prostate cancer.
- The mechanism behind prostasin downregulation and its binding protein (PBP) identity were unknown.
Purpose of the Study:
- Investigate prostasin gene promoter methylation in prostate cancer.
- Identify the prostasin-binding protein (PBP) from seminal vesicles.
- Characterize the interaction between PBP and prostasin.
Main Methods:
- Genomic Southern blot and RT-PCR analyzed prostasin gene promoter and expression.
- Liquid chromatography purified PBP; amino acid sequencing identified it.
- Protease inhibition, binding assays, immunohistochemistry, and Western blot characterized PBP and its interaction with prostasin.
Main Results:
- Prostasin downregulation in prostate cancer cells is partly due to promoter DNA methylation.
- Nerve growth factor (NGF) can induce prostasin expression.
- The PBP was identified as protease nexin-1 (PN-1), a serpin that inhibits prostasin activity and binds to membrane-anchored prostasin.
Conclusions:
- Prostasin expression and function are modulated by the prostate tissue microenvironment.
- Protease nexin-1 (PN-1) plays a role in regulating prostasin activity in prostate cancer.