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

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Data

2019-05-01

Autores

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]

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Resumo

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.

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Palavras-chave

Breast cancer, Gene expression, Nongenomic actions, Thyroid hormone

Como citar

Archives of Endocrinology and Metabolism, v. 63, n. 2, p. 142-147, 2019.

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