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Updated: Aug 6, 2026
Spheroid Assay to Measure TGF-β-induced Invasion
Published on: November 16, 2011
Effect of tamoxifen on transforming growth factor beta1 production by keloid and fetal fibroblasts
A A Mikulec1, M M Hanasono, J Lum
1Division of Otolaryngology/Head and Neck Surgery, Stanford University Medical Center, 300 Pasteur Dr, Stanford, CA 94305-5328, USA.
Background:
Evidence suggests that keloid scar formation may be mediated, in part, by deranged growth factor activity, including that of transforming growth factor (TGF) beta1. Tamoxifen citrate has shown promise in the treatment of keloids.
Objective:
To evaluate the effect of tamoxifen on autocrine growth factor expression in keloid and fetal dermal fibroblasts, which exhibit scar-free healing.
Design:
Serum-free cell lines of keloid and fetal dermal fibroblasts were established. Cell cultures were exposed to different concentrations of tamoxifen solution (8 and 12 or 16 micromol/L). Cell counts were performed and supernatants collected at 24, 48, and 96 hours. Cell-free supernatants were quantitatively assayed for TGF-beta1 expression.
Results:
Keloid fibroblasts show increased per-cell TGF-beta1 production compared with fetal fibroblasts. Tamoxifen appeared to decrease per-cell TGF-beta1 production at each of the time points evaluated.
Conclusions:
Keloids likely arise due to locally insufficient or excessive concentrations of specific growth factors. The higher level of TGF-beta1 produced by keloid cells compared with fetal fibroblasts could be related to the aberrant wound healing seen with keloids. The addition of tamoxifen may lead to improved wound healing in keloids by decreasing the expression of TGF-beta1.
