Human prostatic inhibin suppresses tumor growth and inhibits clonogenic cell survival of a model prostatic adenocarcinoma, the Dunning R3327G rat tumor.
نویسندگان
چکیده
Prostatic inhibin (PI) is a M(r) 10,700 protein found in human seminal plasma and is secreted by the prostate. Recognition of alteration of PI levels in prostatic diseases prompted us to investigate its effect on an animal prostatic adenocarcinoma model, the Dunning R3327G rat tumor. PI not only inhibited in vitro growth of tumor cells but also suppressed tumor growth in vivo. A dose-dependent inhibition of both the clonogenic cell growth and rate of proliferation (DNA synthesis) was observed in tumor cell cultures incubated with purified PI. These inhibitory activities were similar in both androgen-dependent and androgen-independent Dunning tumor cell lines. A functional decapeptide of PI was also found to inhibit Dunning tumor cell colonies in a dose-dependent manner. Daily injection of purified PI into tumor-bearing rats suppressed the tumor growth. A 58% reduction in tumor weight and a 2-fold reduction in tumor growth rate were observed over a 15-day treatment period. Continued treatment with PI significantly suppressed the tumor growth rate by nearly 3-fold. These findings clearly demonstrate a potential application of PI for treating human prostatic adenocarcinoma.
منابع مشابه
Human Prostatic Inhibin Suppresses Tumor Growth and Inhibits Clonogenic Cell Survival of a Model Prostatic Adenocarcinoma, the Dunning R3327G Rat Tumor1
Prostatic inhibin (PI) is a U, 10,700 protein found in human seminal plasma and is secreted by the prostate. Recognition of alteration of PI levels in prostatic diseases prompted us to investigate its effect on an animal prostatic adenocarcinoma model, the Dunning R3327G rat tumor. PI not only inhibited in vitro growth of tumor cells but also suppressed tumor growth in vivo. A dosedependent inh...
متن کاملInhibition of Immune System by an Immunosuppressive Factor from a Human Prostatic Carcinoma Cell Line (JCA-1)
Prostatic carcinoma is the most commonly diagnosed tumor among men over 40 which results in over 30,000 deaths each year in the United States. Previous studies indicated that tumor cell lines produce and release several growth regulatory factors into their condition media and so far a number of human tumor cell-derived suppressor factors have been isolated that affect normal immune functions. I...
متن کاملHORMONAL THERAPY OF PROSTATIC CARCIK:( J?,! 4 : IS THERE A RATIONALE FOR DELAYED TREAT\IE:?:‘l-:;
The report by Huggins and Hodges in 1941’ that endocrine manipulation caused a decrease in acid phosphatase dramatically changed the treatment of metastatic prostatic cancer. Since that time, case reports have clearly described objective responses to hormonal manipulation of this disease.2.3 Nevertheless, although it is generally accepted that hormonal therapy produces subjective remissions in ...
متن کاملEvaluation of c-Myc mRNA Expression Level in Benign Prostatic Hyperplasia and Prostatic Adenocarcinoma Tissues and Its Correlation with Clinicopathological Characteristics
Background and Aims: Prostate cancer (PCa) is one of the most common cancers among men in Iran. Since changes in the regulation of proto-oncogenes expression are the main causes of most human cancers, including PCa, evaluating the expression of marker genes can be helpful for early diagnosis of cancer and better understanding of its etiology. The present study compared c-Myc expression level in...
متن کاملIn Vivo Metabolism of Testosterone-3H in R-3327, an Androgen-sensitive Rat Prostatic Adenocarcinoma1
A spontaneous prostatic adenocarcinoma (R-3327) of a Copenhagen rat has been maintained for 14 generations by s.c. transplantations to Copenhagen and Fi hybrid hosts. The tumor remains histologically a well-differentiated ade nocarcinoma. In order to study the role of gonadal hor mones in this system, tumor expiants were inoculated to intact males, castrated males, and intact females, and the g...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- Cancer research
دوره 53 20 شماره
صفحات -
تاریخ انتشار 1993