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  • Title: Human testicular germ cell tumours express inhibin subunits, activin receptors and follistatin mRNAs.
    Author: van Schaik RH, Wierikx CD, Looijenga LH, Oosterhuis JW, de Jong FH.
    Journal: Br J Cancer; 1997; 76(9):1191-8. PubMed ID: 9365168.
    Abstract:
    Germ cell development is influenced by activin and inhibin, which are produced by Sertoli cells. Activin also affects differentiation of mouse embryonal carcinoma cells, which, to a certain extent, resemble the embryonal carcinoma component of germ cell tumours. Therefore, the expression of inhibin/activin subunits, of activin receptors and of the activin-binding protein follistatin was studied in testicular germ cell tumours, using RNAase protection assays. Testicular germ cell tumours of adolescents and adults (TGCTs) and spermatocytic seminomas expressed activin type I and type II receptors (ActRI and ActRII respectively). Seminomas expressed significantly lower levels of ActRIIA (P<0.05, Mann-Whitney U-test) and higher levels of ActRIA (P<0.05) and ActRIB (P<0.05) compared with non-seminomas. All tumours expressed inhibin beta-subunit transcripts, which are a prerequisite for activin synthesis. Non-seminomas contained significantly higher levels of the inhibin betaA subunit (P<0.001) compared with seminomas. No activin betaC subunit transcripts could be demonstrated by RNAase protection. Inhibin alpha-subunit expression was absent in the spermatocytic seminomas, in six out of nine seminomas and in 10 out of 11 non-seminomas. Follistatin was expressed predominantly in non-seminomas and spermatocytic seminomas. This expression of activin type I and type II receptors in combination with expression of inhibin beta-subunits indicates that activin may act as a para- or autocrine factor in the regulation of growth and differentiation of tumours of human germ cells.
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