| Autor: |
Figueiredo NB; Department of Internal Medicine, Botucatu School of Medicine, University of São Paulo State (UNESP), 18618-000 Botucatu, SP, Brazil., Cestari SH; Department of Internal Medicine, Botucatu School of Medicine, University of São Paulo State (UNESP), 18618-000 Botucatu, SP, Brazil., Conde SJ; Department of Internal Medicine, Botucatu School of Medicine, University of São Paulo State (UNESP), 18618-000 Botucatu, SP, Brazil., Luvizotto RA; Department of Internal Medicine, Botucatu School of Medicine, University of São Paulo State (UNESP), 18618-000 Botucatu, SP, Brazil., De Sibio MT; Department of Internal Medicine, Botucatu School of Medicine, University of São Paulo State (UNESP), 18618-000 Botucatu, SP, Brazil., Perone D; Department of Internal Medicine, Botucatu School of Medicine, University of São Paulo State (UNESP), 18618-000 Botucatu, SP, Brazil., Katayama ML; Department of Radiology, Medicine School, University of São Paulo, USP, 01246-903 São Paulo, SP, Brazil., Carraro DM; Research Center, AC Camargo Hospital, 01509-900 São Paulo, SP, Brazil., Brentani HP; Research Center, AC Camargo Hospital, 01509-900 São Paulo, SP, Brazil., Brentani MM; Research Center, AC Camargo Hospital, 01509-900 São Paulo, SP, Brazil., Nogueira CR; Department of Internal Medicine, Botucatu School of Medicine, University of São Paulo State (UNESP), 18618-000 Botucatu, SP, Brazil ; Department of Clinical Medicine of University of São Paulo State, Rubiao Junior District, s/n, 18618-000 Botucatu, SP, Brazil. |
| Abstrakt: |
It has been well established that estrogen plays an important role in the progression and treatment of breast cancer. However, the role of triiodothyronine (T₃) remains controversial. We have previously shown its capacity to stimulate the development of positive estrogen receptor breast carcinoma, induce the expression of genes (PR, TGF-alpha) normally stimulated by estradiol (E₂), and suppress genes (TGF-beta) normally inhibited by E₂. Since T₃ regulates growth hormones, metabolism, and differentiation, it is important to verify its action on other genes normally induced by E₂. Therefore, we used DNA microarrays to compare gene expression patterns in MCF-7 breast adenocarcinoma cells treated with E₂ and T₃. Several genes were modulated by both E₂ and T₃ in MCF-7 cells (Student's t-test, P < 0.05). Specifically, we found eight genes that were differentially expressed after treatment with both E₂ and T₃, including amphiregulin, fibulin 1, claudin 6, pericentriolar material 1, premature ovarian failure 1B, factor for adipocyte differentiation-104, sterile alpha motif domain containing 9, and likely ortholog of rat vacuole membrane protein 1 (fold change > 2.0, pFDR < 0.05). We confirmed our microarray results by real-time PCR. Our findings reveal that certain genes in MCF-7 cells can be regulated by both E₂ and T₃. |
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