GPR30 is overexpressed in post-puberal testicular germ cell tumors

Franco, Renato; Boscia, Francesca; Gigantino, Vincenzo; Marra, Laura; Esposito, Francesco; Ferrara, Dolores; Pariante, Paolo; Botti, Gerardo; Caraglia, Michele; Minucci, Sergio; Chieffi, Paolo

doi:10.4161/cbt.11.6.14672

Cited by 67 publications

(64 citation statements)

References 26 publications

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“…Some toxic as Atrazine appears to interact strongly with a novel functional oestrogen transmembrane receptor, the G protein-coupled receptor 30 which is overexpressed in postpubertal germ cell tumours. 44,45 Other pathogenic processes could lead to spermatogenic defects. Environmental factors may either damage critical genes or alter gene expression by interfering with the epigenetic programming.…”

Section: Contribution Of Environmental Factorsmentioning

confidence: 99%

Decline of semen quality among 10 932 males consulting for couple infertility over a 20-year period in Marseille, France

Geoffroy-Siraudin¹,

Loundou²,

Romain³

et al. 2012

Asian J Androl

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Semen from 10 932 male partners of infertile couples was analysed and sperm parameter trends were evaluated at the Reproduction Biology Laboratory of the University Hospital of Marseille (France) between 1988 and 2007. After 3-6 days of abstinence, semen samples were collected. Measurements of seminal fluid volume, pH, sperm concentration, total sperm count, motility and detailed morphology of spermatozoa were performed. Sperm parameters were analysed on the entire population and in men with normal total numeration (o40 million per ejaculate). The whole population demonstrated declining trends in sperm concentration (1.5% per year), total sperm count (1.6% per year), total motility (0.4% per year), rapid motility (5.5% per year) and normal morphology (2.2% per year). In the group of selected samples with total normal sperm count, the same trends of sperm quality deterioration with time were observed. Our results clearly indicate that the quality of semen decreased in this population over the study period. Keywords: environment; male infertility; regional differences; semen quality; sperm parameters INTRODUCTION Numerous studies suggest a decline in semen quality in some parts of the world. 1-8 By contrast, other studies have shown no evidence of deteriorating semen quality. 9-16 Some studies concern infertile couples, while others analyse normal sperm parameters. Thus, a worldwide decreasing trend in semen parameter values can be neither confirmed nor rejected. 17 It was recently reported that fecundity is affected by this decrease. 18,19 It was speculated that decreasing sperm parameters are in response to adverse environmental factors. Nevertheless, the observed discrepancies between studies suggest regional differences in semen quality. [20][21][22] Variations in environmental factors, industrial pollution and/or lifestyle could explain these discrepancies. A large number of environmental factors can pollute air, drinking water and food. This can directly alter the male gonad by blood-testis barrier disruption and cellular toxicity, or disrupt androgen biosynthesis and action. Among these environmental factors, oestrogenic or anti-androgenic endocrine disrupting compounds inhibit critical cellular process controlling steroidogenesis in Leydig cells and androgen binding to the androgen receptor. 23 It has been hypothesized that endocrine disrupting compounds play a major role in the aetiology of increased incidence of testicular dysgenesis syndrome which gathers decreased quality of semen, cryptorchidism, hypospadias and testicular cancer. 24 Chemicals with hormone-like activity can also

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Section: Contribution Of Environmental Factorsmentioning

confidence: 99%

Decline of semen quality among 10 932 males consulting for couple infertility over a 20-year period in Marseille, France

Geoffroy-Siraudin¹,

Loundou²,

Romain³

et al. 2012

Asian J Androl

View full text Add to dashboard Cite

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“…In addition, our group has published that GPR30 is over-expressed in human testicular seminomas, which are more often ERα/β negative [8,15,25] .…”

Section: Research Highlightmentioning

confidence: 99%

“…In addition, in our recent published study we have shown by using the TCam2 seminoma cell line that 17β-estradiol induces ERK1/2 activation and c-fos increased expression in absence of ER and in presence of GPR30 [20] . Studies that evaluate GPR30 expression in relation to the classical steroid receptors (ERα/β, PR) and response to chemotherapy are needed to elucidate the value of GPR30 as a prognostic indicator [8,15,27] . Since many G protein-coupled receptors, including GPR30, induce EGFR phosphorylation, the inter-receptor cross-talk demonstrated by this paradigm represents a novel opportunity for therapeutic intervention [28] .…”

Section: Research Highlightmentioning

confidence: 99%

“…It has been well documented in literature that ER is instead down regulated in seminomas and embryonal cell carcinomas [7,12,13] . In the last few years, G protein-coupled receptor 30 (GPR30) was demonstrated to be capable of mediating estrogen actions in a wide variety of cell types including germ cells and Sertoli cells [13][14][15] ; GPR30 has been recently found to bind 17β-estradiol (E2) with high affinity and to mediate estrogenic signals [16,17] controlling the proliferative effects of E2 in ER-negative SKBr3 breast cancer cell lines since GPR30 depletion, by using antisense oligonucleotides or RNA interference (RNAi) strategies, abrogated E2-stimulated growth in these cells [17] . GPR30 activates numerous cell signaling pathways including calcium mobilization, adenylyl cyclase, MAP kinase and phosphatidyl inositol 3-kinase, in large part via the transactivation of epidermal growth factor receptors (EGFRs) [18,19] .…”

Section: Gpr30 Mediates Estrogenic Signalsmentioning

confidence: 99%

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GPR30 is a Potential Therapeutic Target in Human Carcinoma in situ and Seminomas

Chieffi

2015

Receptor Clin Invest

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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 17-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 ER-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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“…Diagnosis is usually based on identification of histological subgroups. In last years, many potential therapeutic targets has been discovered, including SOX2, SOX17, HMGA1, and HMGA 2, Aurora B, PATZ1, GPR30 and others (15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29). Promising molecules capable to selectively target neoplastic cells, that are, serine-threonine kinases, TKs, HMGAs, GPR30 antagonist, proangiogenic factors inhibitors, and micro-RNAs already under clinical evaluation will open a new scenario for TGCTs treatment.…”

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confidence: 99%

GPR30 is overexpressed in post-puberal testicular germ cell tumors

Cited by 67 publications

References 26 publications

Decline of semen quality among 10 932 males consulting for couple infertility over a 20-year period in Marseille, France

Decline of semen quality among 10 932 males consulting for couple infertility over a 20-year period in Marseille, France

GPR30 is a Potential Therapeutic Target in Human Carcinoma in situ and Seminomas

New perspective on molecular markers as promising therapeutic targets in germ cell tumors

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