The etiology and molecular characteristics of Leydig cell tumor (LCT) are scarcely known. From the research data stems that estrogen can be implicated in LCT induction and development, however it is not investigated in detail. Considering the above, herein we analyzed the relation between G-protein coupled membrane estrogen receptor, peroxisome proliferator-activated receptor and insulin-like family peptides (insulin-like 3 peptide; INSL3 and relaxin; RLN) expressions as well as estrogen level with impact of xenoestrogen (bisphenol A; BPA, tetrabromobisphenol A; TBBPA, and tetrachlorobisphenol A; TCBPA). While in our previous studies altered GPER-PPAR partnership was found in human LCT being a possible cause and/or additionally effecting on LCT development, here mouse testes with experimentally induced LCT and mouse tumor Leydig cell (MA-10) treated with BPA chemicals were examined. We revealed either diverse changes in expression or co-expression of GPER and PPAR in mouse LCT as well as in MA-10 cells after BPA analogues when compared to human LCT. Relationships between expression of INSL3, RLN, including co-expression, and estrogen level in human LCT, mouse LCT and MA-10 cells xenoestrogen-treated were found. Moreover, involvement of PI3K-Akt-mTOR pathway or only mTOR in the interactions of examined receptors and hormones was showed. Taken together, species, cell of origin, experimental system used and type of used chemical differences may result in diverse molecular characteristics of LCT. Estrogen/xenoestrogen may play a role in tumor Leydig cell proliferation and biochemical nature but this issue requires further studies. Experimentally-induced LCT in mouse testis and MA-10 cells after BPA exposure seem to be additional models for understanding some aspects of human LCT biology.

中文翻译：

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Leydig细胞肿瘤发生-G蛋白偶联膜雌激素受体，过氧化物酶体增殖物激活受体和异雌激素暴露的影响。体内和体外评估。

Leydig细胞肿瘤（LCT）的病因和分子特征鲜为人知。从研究数据来看，雌激素可能与LCT的诱导和发育有关，但是没有详细研究。考虑到上述情况，本文我们分析了G蛋白偶联膜雌激素受体，过氧化物酶体增殖物激活受体和胰岛素样家族肽（胰岛素样3肽； INSL3和松弛素； RLN）之间的表达以及雌激素水平与影响之间的关系。异雌激素（双酚A； BPA，四溴双酚A； TBBPA和四氯双酚A； TCBPA）。尽管在我们先前的研究中，发现人类LCT中GPER-PPAR伙伴关系的改变可能是导致LCT发展的原因和/或其他影响，在这里，对实验诱导的LCT小鼠睾丸和用BPA化学试剂处理的小鼠肿瘤Leydig细胞（MA-10）进行了检查。我们揭示了与人LCT相比，小鼠LCT以及BPA类似物后MA-10细胞中GPER和PPAR的表达或共表达有多种变化。发现异种雌激素处理的人LCT，小鼠LCT和MA-10细胞中INSL3，RLN的表达（包括共表达）与雌激素水平之间的关系。此外，还显示了PI3K-Akt-mTOR途径或仅mTOR参与了受检受体与激素的相互作用。综上所述，物种，起源细胞，使用的实验系统和使用的化学差异类型可能会导致LCT的分子特性多种多样。雌激素/异雌激素可能在肿瘤Leydig细胞增殖和生化性质中起作用，但是这个问题需要进一步研究。BPA暴露后，小鼠睾丸和MA-10细胞中实验诱导的LCT似乎是了解人类LCT生物学某些方面的其他模型。