AI Article Synopsis
- The study explores how estrogen influences breast cancer by affecting the secretion of stromal cell derived factor-1 (SDF-1).
- Different breast cancer cell lines were treated with varying concentrations of estrogen to assess changes in SDF-1 secretion.
- Results showed that high levels of estrogen significantly increased SDF-1 secretion, which was reversed by estrogen receptor antagonists, indicating that estrogen regulates SDF-1 secretion through its receptor.
Article Abstract
Objective: Stromal cell derived factor-1 (SDF-1) is closely related to the biological characteristics of breast cancer. The aim of this article is to investigate if estrogen affects the biological characteristics of breast cancer via affecting secretion of SDF-1.
Methods: The breast cancer cell lines MCF-7 and MDA-MB-231 used in this study were divided into control group, estrogen group and estrogen plus estrogen receptor (ER) antagonist group. These groups were treated with different concentrations of 17-β estradiol or the same concentration of 17-β estradiol for different times, respectively. Enzyme-linked immunosorbent assay and semi-quantitative reverse transcriptase polymerase chain reaction were performed.
Results: Secretion of SDF-1 was detected in the cell basal medium of MCF-7. When adding a high physiological concentrations of 17-β estradiol (10(-7) mol/L), the levels of SDF-1 secretion achieved a peak at 2 h and it was 6 times of control group (1823.16 ± 325.18 pg/ml comparing to 308.23 ± 9.23 pg/ml, P < 0.01). However, this effect could be eliminated by the pure estrogen antagonist ICI182 or ICI780. The SDF-1 mRNA levels were consistent with the determined SDF-1 protein levels. At the time point of 2 h, for the 10(-7) mol/L group, the SDF-1 mRNA expression levels were higher than the antagonist group, with statistically significant differences (P < 0.05).
Conclusions: It was found that secretion of SDF-1 can be increased by the physiological concentrations of estrogen mainly through regulation of estrogen receptor.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4307513 | PMC |
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