Induction of cell proliferation and survival genes by estradiol-repressed microRNAs in breast cancer cells
1 Department of Pharmacology, School of Chemical Biology & Pharmaceutical Sciences, Capital Medical University, 100069, Beijing, China
2 Institute of Molecular Genetics, College of life science, Hebei United University, TangShan, 063000, China
3 Department of Medical Genetics, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, 72205 USA
BMC Cancer 2012, 12:29 doi:10.1186/1471-2407-12-29Published: 20 January 2012
Additional file 1:
Figure S1. E2 induced the upregulation of bcl-2, cyclinD1 and survivin and moderately suppressed the level of the miRNAs in T47D cells. (A) T47D cells were incubated with phenol red-free IMEM supplemented with 5% charcoal stripped FBS for 48 h. Then cells were treated with vehicle control or 10 nM E2 for 24 and 48 h, total protein was extracted to detect the expression of bcl-2, cyclin D1 and survivin by Western blot. (B) RNA was extracted from the cells and RT-QPCR was used to examine the level of the miRNAs.
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Additional file 2:
Figure S2. E2 induced upregulation of bcl-2, cyclin D1 and survivin at both transcriptional and the post-transcriptional level. (A) MCF-7 cells were pretreated or not with 2 μg/ml actinomycin D for 1 h and then stimulated with 10nM E2 for 12 h. Total protein was extracted to determine the expression of bcl-2, cyclin D1 and survivin. (B) The densitometry of each gene vs. β-actin was indicated and statistical analysis was shown. * denotes P < 0.05 compared with control (the first group).
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