Contribution of various signaling pathways to the cellular senescence process during the development of experimental pituitary tumor

GRONDONA EZEQUIEL; PETITI JP; DE PAUL AL; LUQUES N; GUTIÉRREZ SILVINA; MONGI BRAGATO B; CARREÑO L; TORRES AI

Cordoba

Jornada; XIX Jornada de la Facultad de Ciencias Medicas (JIC); 2018

FCM, UNC

Our data strongly suggests that the cellular senescence process works as a control mechanism of pituitary tumor growth. Previous studies have shownthat the suppression of the PI3K/Akt and ERK 1/2 pathways furthers senescence and that JNK, p38, and nuclear factor kappa B (NF?B) signalingactivation mediates key molecular events that trigger this process. These events regulate the transcription factor FOXO3. Based on these data, weanalyzed the contribution of these signaling pathways to the cellular senescence process during the development of experimental pituitary tumor.To induce pituitary tumor development, adult male Wistar rats were subcutaneously implanted with silastic capsules containing estradiol benzoate (30mg)for 10, 20, 40, and 60 days (E10-60; n = 5). The control group was implanted with empty capsules (n = 5). Then, ERK1/2, Akt, JNK, p38, NF?B, andFOXO3 phosphorylated (p) and total levels were analyzed by Western Blotting and/or inmunohistochemistry across all stages of tumor development. TheANOVA-Fischer test (p