Estrogen-Responsive Genes Overlap with Triiodothyronine-Responsive Genes in a Breast Carcinoma Cell Line

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Figueiredo, Nancy Bueno ; Cestari, Silvia Helena ; Conde, Sandro Jose ; Melo Luvizotto, Renata Azevedo ; De Sibio, Maria Teresa ; Perone, Denise ; Hirata Katayama, Maria Lucia ; Carraro, Dirce Maria ; Brentani, Helena Paula ; Brentani, Maria Mitzi ; Nogueira, Celia Regina

• Tipo de documento: Artigo Científico
• Fonte: SCIENTIFIC WORLD JOURNAL; v. N/A, p. 7-pg., 2014-01-01.

Resumo

It has been well established that estrogen plays an important role in the progression and treatment of breast cancer. However, the role of triiodothyronine (T-3) 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 (E-2), and suppress genes (TGF-beta) normally inhibited by E-2. Since T-3 regulates growth hormones, metabolism, and differentiation, it is important to verify its action on other genes normally induced by E-2. Therefore, we used DNA microarrays to compare gene expression patterns in MCF-7 breast adenocarcinoma cells treated with E-2 and T-3. Several genes were modulated by both E-2 and T-3 in MCF-7 cells (Student's t-test, P < 0.05). Specifically, we found eight genes that were differentially expressed after treatment with both E-2 and T-3, 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 E-2 and T-3. (AU)

• Processo FAPESP: 02/09798-0 - Interrelacao da modulacao genica por estrogeno (e2) e triiodotironina (t3) em adenocarcinoma de mama.
• Beneficiário: Celia Regina Nogueira
• Modalidade de apoio: Auxílio à Pesquisa - Regular