Inhibition of growth and increase of acid phosphatase by testosterone on androgen‐independent murine prostatic cancer cells transfected with androgen receptor cDNA

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Abstract
Most androgen‐unresponsive prostatic cancer cells are found to lack androgen receptor (AR). To clarify the role of AR in the process of the progression from androgen‐dependent to androgen‐unresponsive tumor, the AR gene was transfected into an AR‐negative rat prostatic cancer cell line CUB‐II. AR‐transfectant cells expressed AR mRNA and showed binding to R1881. AR was found in nuclei of AR‐transfectant cells by histochemical examination. Therefore, AR‐transfectant cells were considered to contain functional AR. The growth of AR‐transfectant cells was markedly inhibited in culture in the presence of testosterone, and the effect of testosterone was reduced by simultaneous addition of flutamide. Moreover, tumors inoculated with AR‐transfectant cells in male mice showed much slower growth than those in females. The tumors of AR‐transfectant cells in mice consisted of slightly larger spindle‐shaped cells when compared to those of CUB‐II cells. Moreover, AR‐transfectant cells contained a few polynuclear giant cells. Since CUB‐II cells contained acid phosphatase (AcP) activity, the addition of testosterone in culture increased AcP activity of AR‐transfectant cells. It is concluded that resumption of androgen‐dependent processes reduces the growth rate accompanying changes of phenotype.