Effects of progesterone receptor on proliferation of uterine leiomyoma cells

Shutsung Liao, S Liao, H N Mi, L Y Chai, H N Wang
Journal of biological regulators and homeostatic agents · 2019 · vol. 33(6) , pp. 1685–1693 · doi:10.23812/19-170-a · PMID:31696694 · W3004376565
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This study investigated uterine leiomyoma cells and found that progesterone receptor M promotes cell proliferation by upregulating Caspase-3 and downregulating Bcl-2, while the antagonist Mifepristone inhibited growth.

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This study investigated the role of mitochondrial progesterone receptors in the proliferation of primary uterine leiomyoma cells by extracting and identifying these cells through immunohistochemistry. Researchers utilized Western blotting to screen for various progesterone receptor subtypes and applied the antagonist Mifepristone to observe its effects on cell growth, apoptosis, and protein expression levels of Caspase-3 and Bcl-2. The results demonstrated that increasing concentrations of Mifepristone inhibited cell growth and increased apoptosis rates, while also altering the balance between pro-apoptotic and anti-apoptotic proteins. Furthermore, the paper found that progesterone itself could up-regulate Caspase-3 and down-regulate Bcl-2, thereby inhibiting apoptosis and promoting the proliferation of leiomyoma cells. This paper is centrally about uterine leiomyomas (fibroids); relevance to endometriosis: listed as a related gynecological condition involving progesterone signaling, though the paper's main focus is uterine fibroids.

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Abstract

In order to study the mechanism of the effect of progesterone receptor on the growth of primary uterine leiomyoma cells, the primary cells were extracted from uterine leiomyoma cells and identified by immunohistochemistry (IHC). Mitochondrial progesterone receptor-positive [PR-M(+)], mitochondrial progesterone receptor-negative [PR-M(-)], progesterone receptor A (PR-A) and progesterone receptor B (PR-B) were screened by Western blotting. Different concentrations of Mifepristone (MIF), a progesterone receptor antagonist, were used to interfere with PR-M(+) and PR-M(-) cell lines, respectively. Proliferation and apoptosis of PR-M(+) and PR-M(-) cell lines were detected by tetramethylazolyl blue method and flow cytometry, respectively. The expression of Caspase-3 and B-cell lymphoma 2 (Bcl-2) protein was detected by Western blotting. The results showed that the growth of PR-M(+) and PR-M(-) uterine leiomyoma cells was inhibited with the increase of MIF concentration. Furthermore, the proliferation inhibition rate and apoptosis rate were gradually increased. However, the expression of Caspase-3 protein on progesterone receptor M increased, while the expression of Bcl-2 decreased. Moreover, progesterone could induce progesterone receptor M to up-regulate apoptotic protein Caspase-3 and down-regulate anti-apoptotic protein Bcl-2, thus it could inhibit the apoptosis of primary cultured uterine leiomyoma cells and promote the proliferation of leiomyoma cells.
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Abstract

In order to study the mechanism of the effect of progesterone receptor on the growth of primary uterine leiomyoma cells, the primary cells were extracted from uterine leiomyoma cells and identified by immunohistochemistry (IHC). Mitochondrial progesterone receptor-positive [PR-M(+)], mitochondrial progesterone receptor-negative [PR-M(-)], progesterone receptor A (PR-A) and progesterone receptor B (PR-B) were screened by Western blotting. Different concentrations of Mifepristone (MIF), a progesterone receptor antagonist, were used to interfere with PR-M(+) and PR-M(-) cell lines, respectively. Proliferation and apoptosis of PR-M(+) and PR-M(-) cell lines were detected by tetramethylazolyl blue method and flow cytometry, respectively. The expression of Caspase-3 and B-cell lymphoma 2 (Bcl-2) protein was detected by Western blotting. The results showed that the growth of PR-M(+) and PR-M(-) uterine leiomyoma cells was inhibited with the increase of MIF concentration. Furthermore, the proliferation inhibition rate and apoptosis rate were gradually increased. However, the expression of Caspase-3 protein on progesterone receptor M increased, while the expression of Bcl-2 decreased. Moreover, progesterone could induce progesterone receptor M to up-regulate apoptotic protein Caspase-3 and down-regulate anti-apoptotic protein Bcl-2, thus it could inhibit the apoptosis of primary cultured uterine leiomyoma cells and promote the proliferation of leiomyoma cells.

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References Supporting Agencies Copyright (c) 2019 S. Liao, HN. Mi, LY. Chai, HN. Wang This site is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0). Medical Genetics, University of Torino Medical School, Italy Department of Biomedical, Surgical and Dental Sciences, University of Milan, Italy

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MeSH descriptors

Leiomyoma Receptors, Progesterone Uterine Neoplasms Caspase 3 Caspase 3 Cell Proliferation Cells, Cultured Female Humans Leiomyoma Mifepristone Mifepristone Progesterone Proto-Oncogene Proteins c-bcl-2 Proto-Oncogene Proteins c-bcl-2 Receptors, Progesterone Uterine Neoplasms

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