Figueiredo, Nancy Bueno [UNESP]Cestari, Silvia Helena [UNESP]Conde, Sandro Jose [UNESP]Melo Luvizotto, Renata Azevedo [UNESP]De Sibio, Maria Teresa [UNESP]Perone, Denise [UNESP]Hirata Katayama, Maria LuciaCarraro, Dirce MariaBrentani, Helena PaulaBrentani, Maria MitziNogueira, Célia Regina [UNESP]2014-12-032014-12-032014-01-01Scientific World Journal. New York: Hindawi Publishing Corporation, 7 p., 2014.1537-744Xhttp://hdl.handle.net/11449/112185It 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-3.7engArtigo10.1155/2014/969404WOS:000330657200001Acesso abertoWOS000330657200001.pdf