Abstract
Luteinizing hormone/choriogonadotropin receptor (LHCGR) regulates gonadal testosterone production and recent studies have suggested a growth-regulatory role in somatic cancers. Here, we established that LHCGR is expressed in a fraction of seminoma cells and germ cell neoplasia in situ (GCNIS), and the seminoma-derived cell line TCam2 released LHCGR into the medium. LH treatment induced proliferation of TCam2 cells in vitro, while hCG treatment induced a non-significant 51% increase in volume of tumors formed in a TCam2 xenograft model. A specific ELISA was used to detect a soluble LHCGR in serum. Serum concentrations of soluble LHCGR could not distinguish 4 patients with GCNIS and 216 patients with testicular germ cell tumors (TGCTs) from 297 infertile or 148 healthy young men. Instead, serum LHCGR levels were significantly higher in 112 patients with a seminoma >5 cm or elevated serum lactate dehydrogenase (LDH) compared with men harboring smaller seminomas <2 cm or normal LDH levels. Serum LHCGR levels in TGCT patients could not predict relapse irrespective whether determined pre- or post-orchiectomy. Combined, these novel findings suggest that LHCGR may be directly involved in the progression and growth of seminomas, and our retrospective pilot study suggests that serum LHCGR may have some prognostic value in men with seminoma.
Highlights
Testicular germ cell tumors (TGCTs) represent one of the most common solid tumors in young men [1]
These transcripts were present in normal testis with spermatogenesis (NT), germ cell neoplasia in situ (GCNIS), and seminoma samples (Figure 1A). qPCR showed expression of Luteinizing hormone/choriogonadotropin receptor (LHCGR) in NT, GCNIS, and in specimens with seminoma (Figure 1B)
Presence of LHCGR in GCNIS and seminoma was verified by western blot using three different antibodies targeting different parts of the LHCGR
Summary
Testicular germ cell tumors (TGCTs) represent one of the most common solid tumors in young men [1]. Cancers 2020, 12, 1358 puberty and forms either an invasive seminoma or a non-seminoma [2]. Transition from GCNIS to the more invasive tumors is poorly understood but chromosomal aberrations and endocrine changes are important. This is illustrated by the abrupt rise in TGCT incidence after the pubertal increase in luteinizing hormone (LH), follicle stimulating hormone (FSH), growth hormone, and sex hormone production [3]. Seminoma is associated with elevated levels of lactate dehydrogenase (LDH) but the prognostic potential of this marker is not without flaws since LDH may be elevated in various other non-malignant conditions [6]
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