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-α (ERα) and ERβ subtypes, but only ERβ 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 ERβ 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 ERβ and HMGA1 were observed by using immunoprecipitation and Western blot analyses in combination with immunocytochemistry and immunofluorescence analyses. Here, we show that ERβ interacts with HMGA1 in normal germ cells, while down regulation of ERβ 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 17β-oestradiol induces an HMGA1 increased cytoplasmic expression associated to an ERβ 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 ERβ-mediated growth restraint in human testicular seminoma, probably due to the HMGA1 cytoplasmic delocalization associated with ERβ down-regulation.
| Original language | English |
|---|---|
| Pages (from-to) | 3749-3755 |
| Number of pages | 7 |
| Journal | Journal of Cellular Physiology |
| Volume | 227 |
| Issue number | 12 |
| DOIs | |
| Publication status | Published - Dec 2012 |
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ASJC Scopus subject areas
- Clinical Biochemistry
- Cell Biology
- Physiology
Cite this
The high-mobility group A1-estrogen receptor β nuclear interaction is impaired in human testicular seminomas. / Esposito, Francesco; Boscia, Francesca; Gigantino, Vincenzo; Tornincasa, Mara; Fusco, Alfredo; Franco, Renato; Chieffi, Paolo.
In: Journal of Cellular Physiology, Vol. 227, No. 12, 12.2012, p. 3749-3755.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The high-mobility group A1-estrogen receptor β nuclear interaction is impaired in human testicular seminomas
AU - Esposito, Francesco
AU - Boscia, Francesca
AU - Gigantino, Vincenzo
AU - Tornincasa, Mara
AU - Fusco, Alfredo
AU - Franco, Renato
AU - Chieffi, Paolo
PY - 2012/12
Y1 - 2012/12
N2 - 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-α (ERα) and ERβ subtypes, but only ERβ 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 ERβ 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 ERβ and HMGA1 were observed by using immunoprecipitation and Western blot analyses in combination with immunocytochemistry and immunofluorescence analyses. Here, we show that ERβ interacts with HMGA1 in normal germ cells, while down regulation of ERβ 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 17β-oestradiol induces an HMGA1 increased cytoplasmic expression associated to an ERβ 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 ERβ-mediated growth restraint in human testicular seminoma, probably due to the HMGA1 cytoplasmic delocalization associated with ERβ down-regulation.
AB - 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-α (ERα) and ERβ subtypes, but only ERβ 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 ERβ 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 ERβ and HMGA1 were observed by using immunoprecipitation and Western blot analyses in combination with immunocytochemistry and immunofluorescence analyses. Here, we show that ERβ interacts with HMGA1 in normal germ cells, while down regulation of ERβ 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 17β-oestradiol induces an HMGA1 increased cytoplasmic expression associated to an ERβ 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 ERβ-mediated growth restraint in human testicular seminoma, probably due to the HMGA1 cytoplasmic delocalization associated with ERβ down-regulation.
UR - http://www.scopus.com/inward/record.url?scp=84865420077&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84865420077&partnerID=8YFLogxK
U2 - 10.1002/jcp.24087
DO - 10.1002/jcp.24087
M3 - Article
C2 - 22392906
AN - SCOPUS:84865420077
VL - 227
SP - 3749
EP - 3755
JO - Journal of cellular and comparative physiology
JF - Journal of cellular and comparative physiology
SN - 0021-9541
IS - 12
ER -