Triiodothyronine (T3) upregulates the expression of proto-oncogene TGFA independent of MAPK/ERK pathway activation in the human breast adenocarcinoma cell line, MCF7
Arch. endocrinol. metab. (Online)
; 63(2): 142-147, Mar.-Apr. 2019. graf
Article
in En
| LILACS
| ID: biblio-1001213
Responsible library:
BR1.1
ABSTRACT
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 andmethods:
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.Key words
Full text:
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Index:
LILACS
Main subject:
Triiodothyronine
/
Breast Neoplasms
/
Adenocarcinoma
/
Gene Expression Regulation, Neoplastic
/
Transforming Growth Factor alpha
/
MAP Kinase Signaling System
Limits:
Female
/
Humans
Language:
En
Journal:
Arch. endocrinol. metab. (Online)
Journal subject:
ENDOCRINOLOGIA
/
METABOLISMO
Year:
2019
Type:
Article