Molecular and cellular endocrinology, 2012-03, Vol.350 (1), p.61-71
2012
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- Autor(en) / Beteiligte
- Titel
- Estrogens promote proliferation of the seminoma-like TCam-2 cell line through a GPER-dependent ERα36 induction
- Ist Teil von
- Molecular and cellular endocrinology, 2012-03, Vol.350 (1), p.61-71
- Ort / Verlag
- Ireland: Elsevier Ireland Ltd
- Erscheinungsjahr
- 2012
- Quelle
- Elsevier ScienceDirect Journals
- Beschreibungen/Notizen
- ► Both estradiol and testosterone can stimulate TCam-2 seminoma cell proliferation. ► Estradiol can activate GPER-cAMP/PKA signaling pathway. ► TCam-2 cells can express ERα36, a truncated isoform of the ERα receptor. ► ERα36 expression is rapidly induced after estrogen treatment in a GPER-dependent manner. ► ERα36 is required for estradiol-dependent EGFR expression. Seminoma, originated from carcinoma in situ cells (CIS), is one of the main causes of cancer in young men. Postpubertal development of these testicular germ cell tumors suggests a hormone-sensitive way of CIS cell proliferation induction. Using the unique seminoma TCam-2 cell line, we demonstrate that both estradiol and testosterone can stimulate TCam-2 cell proliferation in the absence of the estradiol receptor ERα. We establish that estradiol can activate GPER-cAMP/PKA signalling pathway. TCam-2 cells express ERα36, a truncated isoform of the canonical ERα receptor, the expression of which is rapidly induced after estrogen treatment in a GPER-dependent manner. ERα36 knockdown indicates that ERα36 is (i) a downstream target of E2-activated GPER/PKA/CREB pathway, (ii) required for estradiol-dependent EGFR expression, (iii) necessary for cell proliferation. Colocalization of ERα36 with cytoskeleton microfilaments suggests a role of estrogens in cell motility. Our results highlight the functional role of ERα36 in context of seminoma cell proliferation and the importance of testing ERα36 in vivo as a possible future prognostic marker.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0303-7207eISSN: 1872-8057, 0303-7207DOI: 10.1016/j.mce.2011.11.021Titel-ID: cdi_hal_primary_oai_HAL_hal_00746506v1
- Format
- –
- Schlagworte
- cAMP-dependent protein kinase, carcinoma, Cell Line, Tumor, cell movement, Cell Nucleus, Cell Nucleus - metabolism, Cell Proliferation, Cyclic AMP, Cyclic AMP - metabolism, Cyclic AMP-Dependent Protein Kinases, Cyclic AMP-Dependent Protein Kinases - metabolism, Cyclin D1, Cyclin D1 - metabolism, Endocrinology and metabolism, ErbB Receptors - genetics, ErbB Receptors - metabolism, ERα36, Estradiol, Estradiol - pharmacology, Estradiol - physiology, Estrogen Receptor alpha, Estrogen Receptor alpha - genetics, Estrogen Receptor alpha - metabolism, estrogen receptors, Estrogens, Estrogens - pharmacology, Estrogens - physiology, Gene Expression, Gene Expression Regulation, germ cells, Human health and pathology, Humans, Life Sciences, Male, men, microfilaments, Phosphorylation, Proliferation, Protein Isoforms, Protein Isoforms - genetics, Protein Isoforms - metabolism, Protein Transport, Receptor, Epidermal Growth Factor, Receptors, Estrogen, Receptors, Estrogen - genetics, Receptors, Estrogen - metabolism, Receptors, G-Protein-Coupled, Receptors, G-Protein-Coupled - genetics, Receptors, G-Protein-Coupled - metabolism, Seminoma, Signal Transduction, TCam-2, testicular development, Testosterone, Testosterone - metabolism, Testosterone - pharmacology, Testosterone - physiology