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The seminoma cell line TCam‐2 is sensitive to HDAC inhibitor depsipeptide but tolerates various other chemotherapeutic drugs and loss of NANOG expression by Daniel Nettersheim; Ad Gillis; Katharina Biermann; Leendert H.J. Looijenga; Hubert Schorle is a Medicine article available to read on EtoBox.
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## Abstract Seminomas and embryonal carcinomas (EC) are both type II germ cell tumor (GCT) entities and develop from the same precursor lesion (carcinoma‐in situ, CIS). However, they show significant differences in growth behavior, differentiation potential, and gene expression. Although ECs are prone to differentiate into all three germ layers and give rise to the non‐seminomatous GCT entities teratoma, choriocarcinoma, and yolk‐sac tumor, differentiation of seminomas to these entities is only rarely observed. This might reflect the ability of seminomas to actively inhibit differentiation processes evoked by environmental cues. Also, it is not known why CIS gives rise to seminoma in some patients and to non‐seminoma in the others. Here, we treated the seminoma‐like cell line TCam‐2 with the HDAC‐inhibitor Depsipeptide, the global demethylating agent 5‐aza‐2′‐deocycytidine, all‐trans retinoic acid and the monaminooxidase inhibitor Tranylcipromine and also used knock down approaches to reduce expression of the pluripotency marker __NANOG__ and/or the inhibitor of primordial germ cell differentiation __TFAP2C__. We found that TCam‐2 cells induce apoptosis when treated with Depsipepti
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- Author
- Daniel Nettersheim; Ad Gillis; Katharina Biermann; Leendert H.J. Looijenga; Hubert Schorle
- Publisher
- John Wiley and Sons; Wiley (John Wiley & Sons); Wiley-Liss Inc; Wiley (ISSN 1045-2257)
- Published
- 2011
- Language
- EN
- Field
- Medicine (Life Sciences)