TNF CONTRIBUTES WITH RAC3-INDUCED MALIGNANT TRANSFORMATION

PANELO L; MARINO GI; COSTAS MA; LIRA MC; RUBIO MF; SOARES MACHADO M; ROSA FD; URTREGER A

Ciudad Autónoma de Buenos Aires

Jornada; XXXIII JORNADAS MULTIDISCIPLINARIAS DE ONCOLOGÍA 2018; 2019

Instituto de Oncología Ángel H. Roffo

RAC3 is a coactivator of steroid receptors and transcription factors and an important oncogene in tumor development. We havepreviously demonstrated that inflammatory cytokines increase theRAC3 expression and that high levels of this molecule could transform non-tumor cells into cancer stem cells. The aim of this workwas to investigate if the inflammatory cytokine TNF could contributeto RAC3 transforming effect, maintaining or increasing stem prop-RESÚMENES DE LAS COMUNICACIONES 147erties. HEK293 cells (human embryonic kidney) overexpressingRAC3 (tumor) or not (non-tumoral) and other tumor cell lines (HeLaand T47D, silencing or not RAC3) were stimulated with TNF (10ng/ml) or vehicle and analyzed for their mesenchymal properties,migratory, invasive behavior and signals that contribute to the stemphenotype. We found that TNF potentiated the RAC3 overexpression effects, increasing the mesenchymal phenotype, through thedecrease of E-cadherin (p