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The (-)-enantiomer of gossypol inhibits proliferation of stromal cells derived from human breast adipose tissues by enhancing transforming growth factor beta1 production.

Yanming ZhangLaboratory of Reproductive and Molecular Endocrinology, College of Veterinary Medicine, Columbus, OH 43210, USASamuel K. KulpLaboratory of Reproductive and Molecular Endocrinology, College of Veterinary Medicine, Columbus, OH 43210, USAY. SugimotoLaboratory of Reproductive and Molecular Endocrinology, College of Veterinary Medicine, Columbus, OH 43210, USARobert W. BrueggemeierLaboratory of Reproductive and Molecular Endocrinology, College of Veterinary Medicine, Columbus, OH 43210, USAYing LinLaboratory of Reproductive and Molecular Endocrinology, College of Veterinary Medicine, Columbus, OH 43210, USA
1998en
ABI

Abstract

We report here that (-)-gossypol significantly inhibits the proliferation of stromal cells derived from human breast adipose tissues (human breast adipose stromal cells) in a dose-dependent manner. The mechanisms involved in the anti-proliferative action of (-)-gossypol on adipose stromal cells were also investigated. (-)-Gossypol stimulated transforming growth factor (TGFbeta1) secretion after 24 h, and RNase protection assay showed that TGFbeta1 mRNA levels were increased as well. We also observed that TGFbeta1 significantly inhibited the growth of human breast adipose stromal cells in a dose-dependent manner. When human breast adipose stromal cells were co-incubated with 5 microM (-)-gossypol and 50 microgram/ml of anti-TGF-beta1,-beta2,-beta3 antibody, growth inhibition caused by (-)-gossypol was completely abrogated. This study indicates that the anti-proliferative activity of (-)-gossypol on human breast adipose stromal cells may be mediated by changes in TGF 1 production.

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