Estrogens promote proliferation of the seminoma-like TCam-2 cell line through a GPER-dependent ERα36 induction
Autor: | Angelina Wallacides, Hussein Ajj, Stéphane Flament, Amand Chesnel, Martine Chillet, Hélène Dumond |
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Přispěvatelé: | Signalisation, Génomique et Recherche Translationnelle en Oncologie (SIGRETO), Université Henri Poincaré - Nancy 1 (UHP) |
Jazyk: | angličtina |
Rok vydání: | 2012 |
Předmět: |
Male
MESH: Signal Transduction MESH: Cyclin D1 Gene Expression MESH: Receptors G-Protein-Coupled MESH: Protein Isoforms Biochemistry MESH: Estrogens Receptors G-Protein-Coupled 0302 clinical medicine Endocrinology Cyclic AMP Protein Isoforms Cyclin D1 Testosterone Phosphorylation Receptor MESH: Estrogen Receptor alpha MESH: Cyclic AMP 0303 health sciences biology Estradiol [SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism MESH: Gene Expression Regulation 3. Good health Seminoma ErbB Receptors Protein Transport Receptors Estrogen 030220 oncology & carcinogenesis MESH: Receptors Estrogen MESH: Estradiol Signal transduction GPER Signal Transduction MESH: Cell Nucleus medicine.medical_specialty MESH: Protein Transport MESH: Cell Line Tumor MESH: Gene Expression medicine.drug_class MESH: Testosterone MESH: Receptor Epidermal Growth Factor MESH: Cyclic AMP-Dependent Protein Kinases CREB 03 medical and health sciences Internal medicine Cell Line Tumor MESH: Cell Proliferation medicine Humans Molecular Biology 030304 developmental biology Cell Proliferation Cell Nucleus MESH: Humans MESH: Phosphorylation Cell growth Estrogen Receptor alpha Estrogens medicine.disease Cyclic AMP-Dependent Protein Kinases MESH: Male Gene Expression Regulation Cell culture Estrogen biology.protein Cancer research MESH: Seminoma |
Zdroj: | Molecular and Cellular Endocrinology Molecular and Cellular Endocrinology, Elsevier, 2012, 350 (1), pp.61-71. ⟨10.1016/j.mce.2011.11.021⟩ |
ISSN: | 0303-7207 |
DOI: | 10.1016/j.mce.2011.11.021⟩ |
Popis: | International audience; 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 E(2)-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. |
Databáze: | OpenAIRE |
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