Cooperative and differential effects of estrogen, prolactin, 22K and 20K human growth hormones on cyclin D1/PRAD1 gene expression in T-47D human breast cancer cells.

Abstract

The cyclin D1/PRAD1 gene is correlated with carcinogenesis of human breast cancer. In this study, we have analyzed effects of breast cancer-related hormones on the cyclin D1 gene expression in T-47D human breast cancer cells. Estradiol (E2) and human prolactin (hPRL) equally enhanced the cyclin D1 gene expression in the cells, and 22 and 20 kDa human growth hormones (22K and 20K hGHs) showed less stimulatory effects. In the presence of E2, however, hPRL or 22K hGH showed additive stimulations of the cyclin D1 gene expression to that by E2 alone, while 20K hGH did not show any additive stimulation of the gene expression. The results suggest that the signal pathways through estrogen and hPRL receptors are important for cyclin D1 gene expression in breast cancer cells, and that 20K hGH has little effect on the cyclin D1 gene expression in these cells because of its lower affinity to PRL receptor.