Abstract
Several studies have demonstrated that the p75NTR low-affinity receptor of Nerve Growth Factor (NGF), is produced in abnormally large amounts in several human cancer types. However, the role of p75NTR varies substantially depending on cell context, so that a dual role of this receptor protein in tumor cell survival and invasion, as well as cell death, has been supported in recent studies. Herein we explored for the first time the expression of p75NTR in human specimens (nr = 40) from testicular germ cell tumors (TGCTs), mostly seminomas. Nuclear overexpression of p75NTR was detected by immunohistochemistry in seminoma tissue as compared to normal tissue, whereas neither NGF nor its high-affinity TrkA receptor was detected. An increased nuclear staining of phospho-JNK, belonging to the p75NTR signaling pathway and its pro-apoptotic target gene, p53, was concomitantly observed. Interestingly, our analysis revealed that decreased expression frequency of p75NTR, p-JNK and p53 was related to staging progression, thus suggesting that p75NTR may represent a specific marker for seminoma and staging in TGCTs.
Highlights
Testicular germ cell tumors (TGCTs) are the most common tumors in adolescents and young men, accounting for almost all testicular cancers and their incidence is rising especially among Caucasians [1]
As reported elsewhere [5], the histogenesis of testicular germ cell tumors (TGCTs) is complex and it is thought that they might develop from premalignant intratubular germ cell neoplasia (IGCN) that progresses toward invasive seminoma and/or non-seminoma after puberty when cells start to proliferate under the influence of hormones [6]
NTR in TGCTs, in testicular seminoma and of its downstream sigsion of p75 molecules, phospho-JNK and p53, whose expression decreases as tumor staging worsens
Summary
Testicular germ cell tumors (TGCTs) are the most common tumors in adolescents and young men, accounting for almost all testicular cancers and their incidence is rising especially among Caucasians [1]. TGCTs are divided into seminoma germ cell tumors (SGCT) and non-seminoma germ cell tumors (NSGCT), the latter including undifferentiated (embryonal carcinoma) or differentiated (teratoma, yolk sac tumor and choriocarcinoma) tumors [2]. As reported elsewhere [5], the histogenesis of TGCTs is complex and it is thought that they might develop from premalignant intratubular germ cell neoplasia (IGCN) that progresses toward invasive seminoma and/or non-seminoma after puberty when cells start to proliferate under the influence of hormones [6]. Since mammalian spermatogenesis is an intricate sequential process of germ cell differentiation from primordial germ cells or spermatogonial stem cells to functional haploid sperm that occurs via a complex interaction between germ and somatic cells, a better knowledge of the regulatory control of spermatogenesis should provide crucial insights into the occurrence and features of TGCTs [8,9,10,11]
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