Artículo
Autocrine IL-6 mediates pituitary tumor senescence
Sapochnik, Melanie Denise
; Haedo, Mariana Raquel
; Fuertes, Mariana
; Ajler, Pablo; Carrizo, Guillermo; Cervio, Andrés; Sevlever, Gustavo; Stalla, Günter K.; Arzt, Eduardo Simon




Fecha de publicación:
01/2017
Editorial:
Impact Journals LLC
Revista:
Oncotarget
ISSN:
1949-2553
Idioma:
Inglés
Tipo de recurso:
Artículo publicado
Resumen
Cellular senescence is a stable proliferative arrest state. Pituitary adenomas are frequent and mostly benign, but the mechanism for this remains unknown. IL-6 is involved in pituitary tumor progression and is produced by the tumoral cells. In a cell autonomous fashion, IL-6 participates in oncogene-induced senescence in transduced human melanocytes. Here we prove that autocrine IL-6 participates in pituitary tumor senescence. Endogenous IL-6 inhibition in somatotroph MtT/S shRNA stable clones results in decreased SA-β-gal activity and p16INK4a but increased pRb, proliferation and invasion. Nude mice injected with IL-6 silenced clones develop tumors contrary to MtT/S wild type that do not, demonstrating that clones that escape senescence are capable of becoming tumorigenic. When endogenous IL-6 is silenced, cell cultures derived from positive SA-β-gal human tumor samples decrease the expression of the senescence marker. Our results establish that IL-6 contributes to maintain senescence by its autocrine action, providing a natural model of IL-6 mediated benign adenoma senescence.
Archivos asociados
https://dx.doi.org/10.18632/oncotarget.13577
http://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=view&path
http://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=view&path

Citación:
Sapochnik, Melanie Denise; Haedo, Mariana Raquel; Fuertes, Mariana; Ajler, Pablo; Carrizo, Guillermo; et al.; Autocrine IL-6 mediates pituitary tumor senescence; Impact Journals LLC; Oncotarget; 8; 3; 1-2017; 4690-4702
Comunidades y colecciones
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Articulos(IBIOBA - MPSP) [134]
Articulos de INST. D/INV.EN BIOMED.DE BS AS-CONICET-INST. PARTNER SOCIEDAD MAX PLANCK