This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by BAHN, R. S. Articles by RABIN, D. Search for Related Content PubMed PubMed Citation Articles by BAHN, R. S. Articles by RABIN, D.

Characterization of Steroid Production in Cultured Human Choriocarcinoma Cells^*

Departments of Medicine and Biochemistry, Vanderbilt University School of Medicine and Veteran's Administration Hospital, Nashville, Tennessee 37232

Address requests for reprints to: Dr. David Rabin, Division of Endocrinology, School of Medicine, Vanderbilt University, Nashville, Tennessee 37232.

Progesterone is the major steroid synthesized by the JEG-3, BeWo, and JAR cell lines of choriocarcinoma. A lesser amount of pregnenolone is produced. The 17a-hydroxy derivatives of these steroids are only minimally present in the three lines. The addition of fetal calf serum to the culture medium modestly increases the synthesis of these steroids, but increases the quantity of 17²-estradiol produced by 30- to 90-fold. The addition of dehydroepiandrosterone, dehydroepian-drosterone sulfate, androstenedione, androstenediol, and testosterone was shown to stimulate 17β-estradiol synthesis. There isa clear dose-response relationship between the amount of testosterone added and the quantity of 17β-estradiol produced. These results indicate that 3β-hydroxysteroid dehydrogenase-isomerase, 17β-ol dehydrogenase, and aromatase are active in cultured choriocarcinoma cells, whereas 17β6-hydroxylase and 17-20-desmolase do not appear to be functional in these cells. It i s concluded that the stereoidogenic capabilities of choriocarci-noma cells in culture are similar to those of the in vivo placenta and support their use as an experimental model of placental steroidogenesis. J Clin Endocrinol Metab 52: 447, 1981)

^* This work was supported by NIH Research Grants HD-10128, HD-92843, HD-05797, and CA-23603 and American Cancer Society Institutional Grant IN-25R-A. Work was performed by R.S.B. in partial fulfillment of Mayo Medical School requirements.

Received August 1, 1980.

This article has been cited by other articles:

				C.-B. Lanz, M. Causevic, C. Heiniger, F. J. Frey, B. M. Frey, and M. G. Mohaupt Fluid Shear Stress Reduces 11{beta}-Hydroxysteroid Dehydrogenase Type 2 Hypertension, January 1, 2001; 37(1): 160 - 169. [Abstract] [Full Text] [PDF]

				X. Ni, S. Luo, T. Minegishi, and C. Peng Activin A in JEG-3 Cells: Potential Role as an Autocrine Regulator of Steroidogenesis in Humans Biol Reprod, May 1, 2000; 62(5): 1224 - 1230. [Abstract] [Full Text]

				A. Kamat, J. L. Alcorn, C. Kunczt, and C. R. Mendelson Characterization of the Regulatory Regions of the Human Aromatase (P450arom) Gene Involved in Placenta-Specific Expression Mol. Endocrinol., November 1, 1998; 12(11): 1764 - 1777. [Abstract] [Full Text]

				Y.-s. Piao, H. Peltoketo, A. Jouppila, and R. Vihko Retinoic Acids Increase 17{beta}-Hydroxysteroid Dehydrogenase Type 1 Expression in JEG-3 and T47D Cells, but the Stimulation Is Potentiated by Epidermal Growth Factor, 12-O-Tetradecanoylphorbol-13-Acetate, and Cyclic Adenosine 3',5'-Monophosphate Only in JEG-3 Cells Endocrinology, March 1, 1997; 138(3): 898 - 904. [Abstract] [Full Text] [PDF]