Paracrine communication between malignant and non-malignant prostate epithelial cells in culture alters growth rate, matrix protease secretion and in vitro invasion
Epithelial cancer cell invasion is facilitated by stromal cells, immune cells, endothelial cells and other epithelial cells. We have used two human papilloma immortalized prostate cell lines, CA-HPV-10 from a carcinoma and PZ-HPV-7 cells from normal prostatic epithelium to study cell-cell influences...
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Published in | Clinical & experimental metastasis Vol. 19; no. 8; pp. 727 - 733 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
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Netherlands
Springer Nature B.V
01.01.2002
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Abstract | Epithelial cancer cell invasion is facilitated by stromal cells, immune cells, endothelial cells and other epithelial cells. We have used two human papilloma immortalized prostate cell lines, CA-HPV-10 from a carcinoma and PZ-HPV-7 cells from normal prostatic epithelium to study cell-cell influences on growth, gelatinase secretion, invasion and responses to TGFbeta1. We found that co-culture with CA-10 carcinoma cells stimulates proliferation of the PZ-7 epithelial line. TGFbeta1 inhibited growth of both lines, but while inhibitory effects on the CA-10 cells diminished after removal of the peptide, inhibition of PZ-7 was lasting. Interestingly, the TGFbeta-induced growth inhibition in PZ-7 cells could be partially reversed by co-culture with CA-10 cells. Co-culture with CA cells in a 3-chamber invasion assay also promoted invasion of PZ cells. CA-10 invasion was enhanced by co-culture with TGFbeta1-treated-PZ-7 cultures and this enhancement was associated with TGFbeta1-induced secretion of matrix metalloproteinase-9. Our observations suggest that interaction between prostate cancer cells and prostate epithelial cells may promote proliferation of the epithelial cell population and produce a paracrine source of MMP-9 which may facilitate early cancer cell invasion. |
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AbstractList | Epithelial cancer cell invasion is facilitated by stromal cells, immune cells, endothelial cells and other epithelial cells. We have used two human papilloma immortalized prostate cell lines, CA-HPV-10 from a carcinoma and PZ-HPV-7 cells from normal prostatic epithelium to study cell-cell influences on growth, gelatinase secretion, invasion and responses to TGFbeta1. We found that co-culture with CA-10 carcinoma cells stimulates proliferation of the PZ-7 epithelial line. TGFbeta1 inhibited growth of both lines, but while inhibitory effects on the CA-10 cells diminished after removal of the peptide, inhibition of PZ-7 was lasting. Interestingly, the TGFbeta-induced growth inhibition in PZ-7 cells could be partially reversed by co-culture with CA-10 cells. Co-culture with CA cells in a 3-chamber invasion assay also promoted invasion of PZ cells. CA-10 invasion was enhanced by co-culture with TGFbeta1-treated-PZ-7 cultures and this enhancement was associated with TGFbeta1-induced secretion of matrix metalloproteinase-9. Our observations suggest that interaction between prostate cancer cells and prostate epithelial cells may promote proliferation of the epithelial cell population and produce a paracrine source of MMP-9 which may facilitate early cancer cell invasion. |
Author | Sehgal, Inder Fischer, William M Greiff, Andrea H |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/12553379$$D View this record in MEDLINE/PubMed |
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SubjectTerms | Cell Communication Cell Division Cell Transformation, Neoplastic Coculture Techniques Culture Media, Conditioned Humans Male Matrix Metalloproteinases - metabolism Neoplasm Invasiveness Prostate - cytology Prostate - pathology Prostate - physiopathology Prostatic Neoplasms - pathology Prostatic Neoplasms - physiopathology Tumor Cells, Cultured |
Title | Paracrine communication between malignant and non-malignant prostate epithelial cells in culture alters growth rate, matrix protease secretion and in vitro invasion |
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