IMR Press / EJGO / Volume 39 / Issue 6 / DOI: 10.12892/ejgo4356.2018

European Journal of Gynaecological Oncology (EJGO) is published by IMR Press from Volume 40 Issue 1 (2019). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with S.O.G.

Open Access Original Research
The impact of progesterone receptor isoforms expression to invasion capacity and SULT1E1 in endometrial cancer cells
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1 Department of Gynecology and Obstetrics, Shengjing Hospital Affiliated of China Medical University, Liaoning, China
2 Department of Gynecology and Obstetrics, the Affiliated Hospital of Inner Mongolia Medical University, Inner Mongolia, China
Eur. J. Gynaecol. Oncol. 2018, 39(6), 953–957;
Published: 10 December 2018

Aim: This study aimed to investigate the mechanism by which progesterone receptors (PRs) mediate in metastatic spread of endometrial cancer (EC). Materials and Methods: The expressions of human progesterone receptor isoforms A and B (hPRA and hPRB) in Ishikawa endometrial cancer cells transfected were examined by Western blot. Matrigel invasion assay was performed to illustrate the roles of hPRA and hPRB in EC metastasis.The underlying mechanism of PR regulating invasion was assessed by Western blot and RT-PCR. Results: In this study ,the authors found a significant increased expression of hPRA and hPRB in transfected cells, respectively, whereas hPRB exhibited a slightly decreased expression upon hPRA stimulation. Matrigel invasion assay demonstrated that hPRB decreased cell invasion, and this process could be largely restored by hPRA treatment. Further study of potential mechanism indicated that hPRB upregulated the expression of SULT1E1, which was connected with endometrial oncogenesis, and the suppression of hPRB via hPRA, exerted an inhibitory effect on the expression of SULT1E1. Conclusions: The above data showed that hPRB promoted the expression of SLUT1E1 to inhibite the invasion of EC cells. In contrast, hPRA played an opposite role in attenuating the effects of hPRB on the invasion of Ishikawa cells and the expression of SLUT1E1.
Endometrial cancer
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