~ DHEA Metabolites and Antiproliferative Action
DHEA Metabolites and Antiproliferative Action
NewsRx.com, March 20, 2003
Antiproliferative action occurs with all DHEA metabolites.
"Dehydroepiandrosterone (DHEA) is a naturally occurring steroid synthesized in the adrenal cortex, gonads, brain, and gastrointestinal tract, and it is known to have chemopreventive and antiproliferative actions on tumors. These effects are considered to be induced by the inhibition of glucose-6-phosphate dehydrogenase (G6PD) and/or HMG-CoA reductase (HMGR) activities," researchers in Japan report.
"The present study was undertaken to investigate whether endogenous DHEA metabolites, i.e. DHEA-sulfate, 7-oxygenated DHEA derivatives, androsterone, epiandrosterone, and etiocholanolone, have antiproliferative effects on cancer cells and to clarify which enzyme, G6PD or HMGR, is responsible for growth inhibition. Growth of Hep G2, Caco-2, and HT-29 cells, evaluated by 3-[4,5-dimethylthiazol]-2yl-2,5-diphenyl tetrazolium bromide (MTT) and bromodeoxyuridine incorporation assays, was time and dose dependently inhibited by addition of all DHEA-related steroids we tested.
"In particular, the growth inhibition due to etiocholanolone was considerably greater than that caused by DHEA in all cell lines. The suppression of growth of the incubated steroids was not correlated with the inhibition of G6PD (r=-0.031, n=9, NS) or HMGR (r=0.219, n=9, NS) activities. The addition of deoxyribonucleosides or mevalonolactone to the medium did not overcome the inhibition of growth induced by DHEA or etiocholanolone, while growth suppression by DHEA was partially prevented by the addition of ribonucleosides. These results demonstrate that endogenous DHEA metabolites also have an antiproliferative action that is not induced by inhibiting G6PD or HMGR activity alone. These nonandrogenic DHEA metabolites may serve as chemopreventive or antiproliferative therapies," wrote S. Yoshida and colleagues.
Yoshida and colleagues published their study in Steroids (Anti-proliferative action of endogenous dehydroepiandrosterone metabolites on human cancer cell lines. Steroids, 2003;68(1):73-83).
The contact person for this report is Y. Matsuzaki, University of Tsukuba, Institute Clinical Med, Department Gastroenterology & Hepatology, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan.
To subscribe to the journal Steroids, contact the publisher: Elsevier Science Inc., 360 Park Avenue South, New York, NY 10010-1710, USA.
The information in this article comes under the major subject areas of Cell Biology, Endocrinology, Etiocholanone, DHEA Metabolites, Hormones, Steroids, Neurology, Gynecology, Antiproliferative Effect, Tumor Growth Suppression, Endogenous Anticarcinogen, Gastroenterology, Nonandrogenic Hormones, Oncology and Antiproliferative Therapy. This article was prepared by Cancer Weekly editors from staff and other reports.
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ęCopyright 2003, Cancer Weekly via NewsRx.com & NewsRx.net
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