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Journal Article

Autocrine IL-6 mediates pituitary tumor senescence

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Stalla,  Günter K.
Dept. Clinical Research, Max Planck Institute of Psychiatry, Max Planck Society;

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Citation

Sapochnik, M., Haedo, M. R., Fuertes, M., Ajler, P., Carrizo, G., Cervio, A., et al. (2017). Autocrine IL-6 mediates pituitary tumor senescence. ONCOTARGET, 8(3), 4690-4702. doi:10.18632/oncotarget.13577.


Cite as: https://hdl.handle.net/21.11116/0000-0001-C92F-9
Abstract
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-beta-gal activity and p16(INK4a) 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-beta-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.