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 tumors. It is well known that estrogens and xenoestrogens are involved in testicular germ cell tumorigenesis. Different studies show that down regulation of estrogen receptor β (ERβ) associates with GPR30 over-expression both in human testicular carcinoma in situ (CIS) and seminomas and that the mitogenic role exerted by 17β-oestradiol induces the activation of extracellular signal-regulated kinase 1/2 (ERK1/2) through GPR30. In conclusion, the exposure to oestrogens or oestrogen-mimics, in some as of yet undefined manner, diminishes the ERβ-mediated growth restraint in CIS and in human testicular seminoma, indicating that GPR30 could be considered a potential therapeutic target to design specific inhibitors.

GPR30: A new potential therapeutic target in human testicular germ cell tumors

Chieffi P.
2021

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 tumors. It is well known that estrogens and xenoestrogens are involved in testicular germ cell tumorigenesis. Different studies show that down regulation of estrogen receptor β (ERβ) associates with GPR30 over-expression both in human testicular carcinoma in situ (CIS) and seminomas and that the mitogenic role exerted by 17β-oestradiol induces the activation of extracellular signal-regulated kinase 1/2 (ERK1/2) through GPR30. In conclusion, the exposure to oestrogens or oestrogen-mimics, in some as of yet undefined manner, diminishes the ERβ-mediated growth restraint in CIS and in human testicular seminoma, indicating that GPR30 could be considered a potential therapeutic target to design specific inhibitors.
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11591/460723
Citazioni
  • ???jsp.display-item.citation.pmc??? 0
  • Scopus 0
  • ???jsp.display-item.citation.isi??? 0
social impact