TCam-2 but not JKT-1 cells resemble seminoma in cell culture

Abstract

Of all malignancies diagnosed in men between 17 and 45 years of age, 60% are germ cell tumors (GCT). GCT arise from carcinoma in situ cells, which are thought to originate from a transformed fetal germ cell, the gonocyte. Seminoma together with embryonal carcinoma represent the most frequent subtypes of GCT. However, the nature of the molecular pathways involved in seminoma formation remains elusive. Therefore, analysis of appropriate cell culture systems is an important prerequisite for further understanding of the etiology of this tumor entity. Although several cell lines for embryonal carcinoma have been established and analyzed, so far only two cell lines from seminoma patients have been reported. In the present study, we have analyzed these seminoma cell lines (TCam-2 and JKT-1) and compared the gene-expression profiles with those of normal tissue and of seminoma and embryonal carcinoma by using DNA Array technology. We have found that TCam-2 clusters with the group of classical seminoma, whereas JKT-1 clusters with the group of embryonal carcinoma. Using reverse transcription/polymerase chain reaction, Western blot, and immunohistochemistry, we have confirmed the seminoma-like nature of TCam-2, whereas JKT-1 lacks expression for most of the genes detectable in GCTs, thus making doubtful the germ cell nature of this cell line. The data represent the first genome-wide expression analysis of the two cell lines and comparison/clustering with subgroups of germ cell tumors. Only TCam-2 seems to represent a suitable in vitro model for seminoma.

NANOG promoter methylation and expression correlation during normal and malignant human germ cell development

“…Alternatively, the data for JKT-1, together with experiments from us and others, further indicate that JKT-1 does not (or no longer) display seminoma-like characteristics. 25,26 To address the question whether NANOG expression correlates to methylation of the CpGs in the NRR in GCTs and derived cell lines, we performed qRT-PCR analysis. NANOG expression levels were high in seminomas and embryonal carcinomas, while low and absent in teratomas, yolk sac tumors, choriocarcinomas and mixed non-seminomas (Fig.…”

The seminoma cell line TCam‐2 is sensitive to HDAC inhibitor depsipeptide but tolerates various other chemotherapeutic drugs and loss of NANOG expression

“…It is postulated that seminomas are not able to differentiate in vivo (Battifora et al, 1984;Srigley et al, 1988), although some rare cases of seminomatous in vivo differentiation were described (Czaja and Ulbright, 1992) and a transition step to ECs is hypothesized (Oosterhuis and Looijenga, 2005 #23). The TCam-2 cell line resembles a seminoma since it expresses markers of primordial germ cells (PGC) and seminomas as well as markers indicative for pluripotency and self-renewal (KIT, TFAP2C, BLIMP1, VASA, GDF3, MCFD2, D2-40, SOX17, NANOG, OCT3/4) (de Jong et al, 2008a;Eckert et al, 2008). Alike seminomas, TCam-2 cells lack expression of SOX2 but are positive for SOX17 (de Jong et al, 2008b).…”

Estrogen receptor beta (ERβ) produces autophagy and necroptosis in human seminoma cell line through the binding of the Sp1 on the phosphatase and tensin homolog deleted from chromosome 10 (PTEN) promoter gene

“…20 In this study, we focused on SE using the TCAM2 cell lines containing typical features of human SE. 21 We aimed to investigate a functional link between the ERβ and PTEN and evidenced that E2 induced PTEN expression, defining the molecular mechanism. We propose that PTEN might be one of the signaling proteins on which E2 is acting to affect seminoma cell survival.…”