Abstract
The G protein-coupled estrogen receptor (GPR30) is suggested to exert a role in non-nuclear estrogen signalling and is over-expressed in a variety of hormone dependent cancer entities. It is well established that oestrogens are involved in testicular germ cell tumours. In a recent paper published in Journal of Cellular Physiology, we show that down regulation of estrogen receptor β (ERβ) associates with GPR30 over-expression both in human testicular carcinoma in situ (CIS) and seminomas. In addition, we demonstrate that 17b-oestradiol induces the ERK1/2 activation through GPR30. The results suggested that exposure to oestrogens or oestrogen-mimics, in some as of yet undefined manner, diminishes the ERb-mediated growth restraint in CIS and in human testicular seminoma, indicating that GPR30 could be a potential therapeutic target to design specific inhibitors.
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