Triiodothyronine (T3) upregulates the expression of proto-oncogene TGFA independent of MAPK/ERK pathway activation in the human breast adenocarcinoma cell line, MCF7

• Autor(a) principal: Silva,Tabata M.
• Data de Publicação: 2019
• Outros Autores: Moretto,Fernanda C. F., Sibio,Maria T. De, Gonçalves,Bianca M., Oliveira,Miriane, Olimpio,Regiane M. C., Oliveira,Diego A. M., Costa,Sarah M. B., Deprá,Igor C., Namba,Vickeline, Nunes,Maria T., Nogueira,Célia R.
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Arquivos de Endocrinologia e Metabolismo (Online)
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S2359-39972019000200142
• topic: Thyroid hormone; nongenomic actions; gene expression; breast cancer

ABSTRACT Objective: 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.