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GPR30: A new potential therapeutic target in human testicular germ cell tumors
1Dipartimento di Psicologia, Università della Campania, Caserta, Italy.
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.
Insights
Estrogen signaling via G protein-coupled estrogen receptor (GPR30) may promote testicular cancers by overriding growth restraint. GPR30 is a potential therapeutic target for inhibiting these hormone-dependent tumors.
Area of Science:
- Endocrinology
- Oncology
- Molecular Biology
Background:
- G protein-coupled estrogen receptor (GPR30) mediates non-nuclear estrogen signaling.
- Estrogens and xenoestrogens are implicated in testicular germ cell tumorigenesis.
- GPR30 is over-expressed in various hormone-dependent tumors.
Purpose of the Study:
- To investigate the role of GPR30 in testicular cancer.
- To explore the relationship between GPR30, estrogen receptor beta (ERβ), and tumor growth.
- To examine the activation of extracellular signal-regulated kinase 1/2 (ERK1/2) pathway.
Main Methods:
- Analysis of GPR30 and ERβ expression in human testicular carcinoma in situ (CIS) and seminomas.
- Investigating the mitogenic effects of 17β-oestradiol.
- Assessing ERK1/2 activation through GPR30 signaling.
Main Results:
- Down-regulation of ERβ correlates with GPR30 over-expression in human testicular CIS and seminomas.
- 17β-oestradiol-induced mitogenesis activates ERK1/2 via GPR30.
- Estrogen exposure diminishes ERβ-mediated growth restraint in testicular cancer.
Conclusions:
- GPR30 plays a significant role in testicular tumorigenesis.
- GPR30 may override ERβ-mediated growth inhibition in testicular cancer.
- GPR30 represents a potential therapeutic target for specific inhibitors in hormone-dependent testicular tumors.
