TNF CONTRIBUTES WITH RAC3-INDUCED MALIGNANT TRANSFORMATION

MILENI SOARES MACHADO; LAURA PANELO; MARÍA CECILIA LIRA; FRANCISCO DAMIÁN ROSA; GABRIELA INÉS MARINO; MARÍA FERNANDA RUBIO; ALEJANDRO URTREGER; MÓNICA ALEJANDRA COSTAS

Mar del Plata

Congreso; LXIII Reunión Anual de la Sociedad Argentina de Investigación Clínica; 2018

SAIC

RAC3 is a coactivator of steroid receptors and transcription factorsand an important oncogene in tumor development. We havepreviously demonstrated that inflammatory cytokines increase theRAC3 expression and that high levels of this molecule could transformnon-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 propRAC3 (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 overexpressioneffects, increasing the mesenchymal phenotype, through thedecrease of E-cadherin (p