TNF contributes with RAC3-induced malignant transformation

SOARES MACHADO M; PANELO L.C.; LIRA, M C; ROSA, F D; MARINO, GABRIELA; RUBIO M. F.; URTREGER A; COSTAS M. A.

Mar Del Plata

Congreso; Reunión Anual de la SAIC; 2018

SAIC-SAI-SAFIS

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