Hum. Reprod. Advance Access originally published online on February 15, 2008
Human Reproduction 2008 23(4):775-782; doi:10.1093/humrep/den010
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Presumed pluripotency markers UTF-1 and REX-1 are expressed in human adult testes and germ cell neoplasms
1 University Department of Growth and Reproduction, Section GR5064, Rigshospitalet, Blegdamsvej 9, 2100 Copenhagen, Denmark 2 Department of Pathology, Rigshospitalet, Blegdamsvej 9, 2100 Copenhagen, Denmark
3 Correspondence address. E-mail: moebjerg{at}imbg.ku.dk
BACKGROUND: UTF-1 and REX-1/ZFP42 are transcription factors involved in pluripotency. Because of phenotypic similarities between pluripotent embryonic stem cells and testicular germ cell tumours (TGCT) and the derivation of pluripotent cells from testes, we investigated the expression of UTF-1 and REX-1 during human gonadal development and in TGCT.
METHODS: Expression of UTF-1 and REX-1 was studied in 52 specimens from human gonadal development and in 86 samples from TGCT.
RESULTS: UTF-1 and REX-1 were expressed throughout male gonadal development. In the mature testis, UTF-1 was expressed in spermatogonia, whereas REX-1 was expressed in meiotic cells and, together with OCT-3/4, in primary oocytes. Both UTF-1 and REX-1 were expressed in testicular carcinoma in situ and in TGCT. Contrarily to REX-1, UTF-1 was expressed in all spermatocytic seminomas.
CONCLUSIONS: Unlike other pluripotency markers NANOG and OCT-3/4, UTF-1 and REX-1 are expressed throughout human testes development. The expression pattern indicated that UTF-1 plays a possible role in spermatogonial self-renewal, whereas expression of REX-1 in meiotic cells from both testes and ovary indicate a role in meiosis. UFT-1 and REX-1 are expressed in TGCT and the high abundance of UTF-1 in spermatocytic seminomas is consistent with the hypothesis that this tumour type originates from spermatogonia.
Key words: germ cell differentiation/pluripotency/UTF-1/REX-1/germ cell neoplasms
Submitted on September 19, 2007; resubmitted on October 24, 2007; accepted on December 5, 2007.