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Density dependent polarized secretion of a prostatic epithelial cell line
D Djakiew1, B Pflug, R Delsite
1Department of Anatomy and Cell Biology, Georgetown University Medical Center, Washington, D.C.
The Prostate
|January 1, 1992
Summary
Prostatic epithelial cells (PA-III) show altered protein and protease secretion when cultured in fetal calf serum (FCS), mimicking an anaplastic phenotype. This loss of polarized secretion may facilitate tissue degradation in vivo.
Area of Science:
- Cell Biology
- Biochemistry
- Cancer Research
Background:
- Prostatic epithelial cells (PA-III) exhibit polarized secretion of proteins and proteases.
- The anaplastic phenotype is associated with a loss of cellular polarity.
- Understanding secretion polarity is crucial for cancer progression research.
Purpose of the Study:
- To investigate the polarized secretion of total protein and proteases in PA-III cells under different culture conditions.
- To compare the secretory patterns of normal and anaplastic-like PA-III cells.
- To correlate the loss of polarized secretion with the anaplastic phenotype.
Main Methods:
- PA-III cells cultured in dual compartment chambers with or without fetal calf serum (FCS).
- Analysis of 35S-methionine labeled total protein secretion.
- Quantification of protease secretion (metalloproteinases, t-PA, gelatinases, urokinase) in apical and basal compartments.
Main Results:
- PA-III cells in serum-free defined medium (SFDM) showed predominantly apical secretion of total protein.
- PA-III cells in FCS exhibited inverted polarity, with increased basal secretion of total protein.
- Protease secretion polarity was inverted in FCS, with basal secretion of metalloproteinases, t-PA, and gelatinases, suggesting a functional loss of polarity.
Conclusions:
- The anaplastic phenotype in PA-III cells is characterized by a loss or inversion of polarized secretion.
- Altered protease secretion may contribute to basement membrane and tissue degradation in vivo.
- This study provides insights into the functional consequences of disrupted cell polarity in cancer.