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GPER1 in the thyroid: A systematic review
Patrícia de Araujo Manfroi1, Ana Paula Santin Bertoni2, Tania Weber Furlanetto3
1Postgraduate Program in Medicine: Medical Sciences, School of Medicine, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil.
Background:
Thyroid cancer incidence has been increasing, acquiring a greater importance in health, especially of women, who are more frequently affected. As 17-β-estradiol (E2) has been shown to have a proliferative effect on benign and malignant thyroid cells, G protein-coupled estrogen receptor (GPER1) could have a role on the pathogenesis of thyroid cancer.
Objective:
To evaluate data on GPER1 in the thyroid.
Data Sources:
PubMed, Scielo and Cochrane Library databases were searched, using the keywords GPER1 or GPR30 or GPER and thyroid, since the inception until Jun, 2019. Other sources were used, as cross-referencing.
Study Selection:
All studies which evaluated GPER1 GPER1 or GPR30 or GPER in the thyroid.
Data Extraction:
From 23 articles identified, eight studies were included: one in commercial samples of human thyroid, four in human thyroid cancer cell lines, and three in human samples of benign and/or malignant thyroid diseases.
Data Synthesis:
GPER1 gene and protein expression were described, respectively, in six and five studies, and the results varied according to the study. In three studies, increased proliferation of four thyroid cancer cell lines were induced by E2, with evidences suggesting that GPER1 at least partially mediated growth in these cells. GPER1 was identified in the cell membrane, in three studies, and in the cytoplasm in two studies.
Conclusions:
The paucity of studies about GPER1 in the thyroid, as well as methodological differences between them, precludes firm conclusions about GPER1 role in the thyroid, although there are some evidences of GPER1-induced proliferation of thyroid cancer cells.
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