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Establishment of an androgen‐responsive prostatic cell line “PEA5” from a p53‐deficient mouse
Author(s) -
Hanazono Makoto,
Nozawa Rie,
Itakura Reiko,
Aizawa Shinichi,
Tomooka Yasuhiro
Publication year - 2001
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/1097-0045(20010215)46:3<214::aid-pros1026>3.0.co;2-0
Subject(s) - androgen , cell culture , androgen receptor , endocrinology , dihydrotestosterone , prostate , medicine , biology , transferrin , cell growth , prostate cancer , hormone , cancer , biochemistry , genetics
Background We demonstrated that p53‐deficiency is sufficient for the establishment of clonal cell lines from the uterus and prostate. In the present study, we improved cloning methods to establish androgen‐responsive cell lines. Methods In our previous study, a prostatic cell line was established from the ventral prostate of a p53‐deficient mouse and was maintained in a medium containing heat‐inactivated fetal calf serum at 10% supplemented with insulin (10 μg/ml), transferrin (10 μg/ml), cholera toxin (10 ng/ml) and selenium (10 −8 M). In the present study, 5α‐dihydrotestosterone (10 −8 M) was added to the medium from the beginning of cloning procedures. Results We succeeded in the establishment of an androgen receptor positive prostatic cell line, designated PEA5. PEA5 cells exhibited a typical epithelial morphology in culture and growth was stimulated by androgens in a dose‐dependent manner. In addition, they grew and formed three‐dimensional structures in collagen gel, in which growth was also stimulated by androgen. Conclusions Although PEA5 lacks p53 gene, it still retains androgen sensitivity. In collagen gel culture, PEA5 cells can grow and form three‐dimensional structures similar to those of the primary cultures reported previously. Furthermore, prostates of p53‐deficient mice are shown to be useful sources for obtaining androgen‐responsive cells lines. Prostate 46:214–225, 2001. © 2001 Wiley‐Liss, Inc.