http://www.cnr.it/ontology/cnr/individuo/prodotto/ID206819
The high-mobility group A1-estrogen receptor ? nuclear interaction is impaired in human testicular seminomas. (Articolo in rivista)
- Type
- Label
- The high-mobility group A1-estrogen receptor ? nuclear interaction is impaired in human testicular seminomas. (Articolo in rivista) (literal)
- Anno
- 2012-01-01T00:00:00+01:00 (literal)
- Alternative label
Esposito F, Boscia F, Gigantino V, Tornincasa M, Fusco A, Franco R, Chieffi P. (2012)
The high-mobility group A1-estrogen receptor ? nuclear interaction is impaired in human testicular seminomas.
in Journal of cellular physiology (Print)
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Esposito F, Boscia F, Gigantino V, Tornincasa M, Fusco A, Franco R, Chieffi P. (literal)
- Rivista
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- Dipartimento di Medicina Sperimentale, II Università di Napoli, Via Costantinopoli, Naples, Italy.
Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche (IEOS-CNR), Napoli 80131, Italy. (literal)
- Titolo
- The high-mobility group A1-estrogen receptor ? nuclear interaction is impaired in human testicular seminomas. (literal)
- Abstract
- It is well established that estrogens participate in the control of normal spermatogenesis and endogenous or environmental estrogens are involved in pathological germ cell proliferation including testicular germ cell tumors. The effects of estrogen are now known to be mediated by estrogen receptor-? (ER?) and ER? subtypes, but only ER? has been found in human germ cells of normal testis. However, its expression was markedly diminished in human testicular seminomas. The expression and the possible interaction of ER? and HMGA1 were studied in normal germ cells and in human testicular seminomas. GC1 and TCam-2 germ cell lines, were used; in addition, a tissue micro-array (TMA) was built using the most representative areas from 35 cases of human testicular seminomas. The expression and the interaction of ER? and HMGA1 were observed by using immunoprecipitation and Western blot analyses in combination with immunocytochemistry and immunofluorescence analyses. Here, we show that ER? interacts with HMGA1 in normal germ cells, while down regulation of ER? associates with transcriptional co-regulator HMGA1 over-expression and cytoplasmic localization both in human testicular seminomas and in TCam-2 cell line. In addition, we show that 17?-oestradiol induces an HMGA1 increased cytoplasmic expression associated to an ER? down-regulation in TCam-2 cell line. Taken together, our results suggest that exposure to estrogens or estrogen-mimics, in some as of yet undefined manner, diminishes the ER?-mediated growth restraint in human testicular seminoma, probably due to the HMGA1 cytoplasmic delocalization associated with ER? down-regulation. (literal)
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