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Growth of HPV-18 immortalized human prostatic intraepithelial neoplasia cell lines. Influence of IL-10, follistatin, activin-A, and DHT
Journal article

Growth of HPV-18 immortalized human prostatic intraepithelial neoplasia cell lines. Influence of IL-10, follistatin, activin-A, and DHT

M Wang, A Liu, F U Garcia, J S Rhim and M E Stearns
International journal of oncology, v 14(6), pp 1185-1195
Jun 1999
DOI: https://doi.org/10.3892/ijo.14.6.1185
PMID: 10339677
Featured in Collection :   UN Sustainable Development Goals @ Drexel

Abstract

Activins Adjuvants, Immunologic - pharmacology Androgens - physiology Animals Blotting, Western Cell Adhesion - physiology Cell Division - drug effects Cell Line, Transformed Cell Transformation, Viral Colony-Forming Units Assay Dehydroepiandrosterone - pharmacology Dihydrotestosterone - pharmacology Enzyme-Linked Immunosorbent Assay Follistatin Glycoproteins - pharmacology Growth Substances - pharmacology Humans Inhibins - pharmacology Interleukin-10 - pharmacology Light Male Mice Mice, SCID Microscopy Papillomaviridae Prostatic Intraepithelial Neoplasia - pathology Prostatic Intraepithelial Neoplasia - virology Prostatic Neoplasms - pathology Prostatic Neoplasms - virology Tumor Cells, Cultured
Cultures from high grade prostatic intraepithelial neoplasia (HGPIN) have been established and immortalized by HPV-18 infection. The cultures were identified as PIN by Western blotting with anti-cytokeratin (34betaE12) and prostate specific antigen (PSA) antibodies. We examined the growth capabilities of the cultures in the presence of TGF-beta1, activin-A, follistatin (FS), androgens (DHEA, DHT) and several cytokines (IL-10, IL-2, IL-4). IL-10, FS, and DHT stimulated cell proliferation and colony forming ability, while the other cytokines and growth factors had no discernable effect. In addition, DHT and to a lesser extent IL-10 both stimulated PSA production. Activin-A blocked IL-10, FS, and DHT stimulated growth and PSA production. We interpret the data to mean that IL-10 induction of FS secretion (and FS binding of activin A) restores the normal growth capabilities of HGPIN cultures.

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Collaboration types
Domestic collaboration
Web of Science research areas
Oncology
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