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

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.

Keywords
Thyroid hormone; nongenomic actions; gene expression; breast cancer