Contribution of different signaling pathways on the development of estrogen-induced pituitary tumors: their role in senescence process

LILIANA DEL VALLE SOSA; SILVINA GUTIÉRREZ; EZEQUIEL GRONDONA; JUAN PETITI; ANA L DE PAUL; MONGI BRAGATO BETHANIA; LUCÍA CARREÑO; ALICIA TORRES

Buenos Aires

Congreso; Reunión Conjunta de Sociedades de Biociencias; 2017

SAIC

Recently we demonstrated signs of cellular senescence as a growth control mechanism during the progression of experimental pituitary tumors. Also, it is known that Ras induces negative feedback response on PI3K/Akt and ERK1/2 pathways, thus promoting senescence. Oppositely, JNK and p38-stress signalling activation mediates key molecular events triggering the senescence program. Based on these evidences, we evaluated the contribution these signalling pathways on cellular senescence during the development of estrogen-induced pituitary tumors.To induce pituitary tumors, Wistar adult male rats were implanted with silastic capsules containing estradiol benzoate (30mg) for 10, 20, 40 and 60 days (E10-60). Control group was implanted with empty capsules. Subsequently, phosphorylated (p) and total ERK1/2; AKT; JNK and p38 protein levels were determined by Western blot. Also, pERK1/2, pAKT and senescent associated-b-Galactosidase (SA-b-gal) double staining was performed in cryosections from normal and tumoral pituitaries. Statistical analysis: ANOVA-Fischer test (p