Retinol Esterification in Human Breast Cancer Cells
Abstract
This study was designed to identify the RA target genes in the normal human mammary epithelial cells (HMEC) and breast cancer cells. We found that the IL-1Beta gene was an early responsive gene and its expression was up-regulated as early as two hours after RA treatment. Results from the treatment of HMEC with cycloheximide and actinomycin D indicated that the expression of the IL-1Beta gene was regulated by RA at the transcriptional level and that the regulation does not require the concurrent protein synthesis. Either RA or IL-1Beta could significantly inhibit the proliferation of HMEC. However, the addition of soluble IL-1 receptor antagonist (sIL-1ra) to the cell culture medium did not block RA-induced EMEC growth inhibition, whereas sIL-1ra blocked the growth inhibition of HMEC by IL-1Beta. The basal IL-1Beta expression was lost in the human breast carcinoma MCF-7, MDA-MB-231 and MDA-MH-468 cell lines. The strong inhibitory effects of RA and IL-1Beta on the growth of the estrogen receptor (ER) positive NCF-7 cell line were shown, but only a small effect on the ER negative MDA-MB-231 cells was found. Our study supports the hypothesis that the co-administration of IL-1Beta may enhance the therapeutic effect of RA on certain breast cancers.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jan 01, 2002
- Accession Number
- ADA405293
Entities
People
- Limin Liu
Organizations
- Weill Cornell Medicine