Triiodothyronine (T 3 ) upregulates the expression of proto-oncogene TGFA independent of MAPK/ERK pathway activation in the human breast adenocarcinoma cell line, MCF7

摘要

Objective: To verify the physiological action of triiodothyronine T 3 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 T 3 at a physiological dose (10 ?9 M) 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: T 3 increases the expression of TGFA mRNA in MCF7 cells in 4 h of treatment. Inhibition of RNA polymerase II modulates the effect of T 3 treatment on the expression of TGFA in MCF7 cells. Activation of the MAPK/ERK pathway is not required for T 3 to affect the expression of TGFA mRNA. Conclusion: Treatment with a physiological concentration of T 3 after RNA polymerase II inhibition altered the expression of TGFA . Inhibition of the MAPK/ERK pathway after T 3 treatment does not interfere with the TGFA gene expression in a breast adenocarcinoma cell line.