Silva, Tabata M. [UNESP]Moretto, Fernanda C. F. [UNESP]De Sibio, Maria T. [UNESP]Gonçalves, Bianca M. [UNESP]Oliveira, Miriane [UNESP]Olimpio, Regiane M. C. [UNESP]Oliveira, Diego A. M. [UNESP]Costa, Sarah M. B. [UNESP]Deprá, Igor C. [UNESP]Namba, Vickeline [UNESP]Nunes, Maria T.Nogueira, Célia R. [UNESP]2019-10-062019-10-062019-05-01Archives of Endocrinology and Metabolism, v. 63, n. 2, p. 142-147, 2019.2359-42922359-3997http://hdl.handle.net/11449/187698Objective: To verify the physiological action of triiodothyronine T3 on the expression of transforming growth factor α (TGFA) mRNA in MCF7 cells by inhibition of RNA Polymerase II and the MAPK/ERK pathway. Materials and methods: The cell line was treated with T3 at a physiological dose (10-9M) for 10 minutes, 1 and 4 hour (h) in the presence or absence of the inhibitors, α-amanitin (RNA polymerase II inhibitor) and PD98059 (MAPK/ERK pathway inhibitor). TGFA mRNA expression was analyzed by RT-PCR. For data analysis, we used ANOVA, complemented with the Tukey test and Student t-test, with a minimum significance of 5%. Results: T3 increases the expression of TGFA mRNA in MCF7 cells in 4 h of treatment. Inhibition of RNA polymerase II modulates the effect of T3 treatment on the expression of TGFA in MCF7 cells. Activation of the MAPK/ERK pathway is not required for T3 to affect the expression of TGFA mRNA. Conclusion: Treatment with a physiological concentration of T3 after RNA polymerase II inhibition altered the expression of TGFA. Inhibition of the MAPK/ERK pathway after T3 treatment does not interfere with the TGFA gene expression in a breast adenocarcinoma cell line.142-147engBreast cancerGene expressionNongenomic actionsThyroid hormoneArtigo10.20945/2359-3997000000114S2359-39972019000200142Acesso aberto2-s2.0-85066163660S2359-39972019000200142.pdf