AMPLIFICATION OF PITUITARY TUMOR SENESCENCE BY IL-6: A MECHANISM TO CONTROL TUMOR EXPANSION

FLORENCIA HERBSTEIN; MELANIE SAPOCHNIK; DAVID GONILSKI PACIN; NICOLÁS CIANCIO DEL GIUDICE; MANUEL FIZ; ALEJANDRA ATTORRESI; CORA POLLAK; SERGIO SENIN; MARÍA BELÉN ELGUERO; MARIANA FUERTES; LUCAS B. PONTEL; EDUARDO ARZT

Mar del Plata

Congreso; LXVIII Reunión Anual de la Sociedad Argentina de Investigación Clínica; 2023

Sociedad Argentina de Investigación Clínica (SAIC)

IL-6 is a pleiotropic cytokine of the senescence-associated secretory phenotype (SASP) that has antagonistic actions. IL-6 canonical signaling via STAT3 induces proliferation when it interacts with the membrane receptor, IL-6R. Pituitary adenomas are common, benign tumors characterized by premature proliferative arrest, in which the activation of the cellular senescence program emerges as a mechanism to explain these features. In previous studies, we demonstrated that IL-6 increases senescence in a senescent pituitary cell line, indicating that the origin of IL-6 is crucial for its action. To analyze this mechanism of action of IL-6, we studied the secretion-independent effects of IL-6 in two cellular models of senescence: Pituitary MtT/S cells and doxorubicin-induced senescent A549 cells. In both we observed an increase in senescence biomarkers (p16Ink4/p21Cip1 and pRb, p