TNF-induced up-regulation of RAC3 expression elicits a pro-inflammatory profile in breast cancer-associated adipocytes.

IGNASIO AIELLO; JULIANA LOURDES BERNACCHIA; NATALIA PALADINO; FRANCISCO DAMIÁN ROSA; IARA CASTELLANOS; MARÍA CECILIA SALAZAR GÜEMES; MARÍA FERNANDA RUBIO; LIRA, MARÍA CECILIA; MILENI SOARES MACHADO; ALEJANDRA GRACIELA PALMA; MÓNICA ALEJANDRA COSTAS

Mar del Plata

Congreso; Reunión Anual de Sociedades de Biociencias 2022; 2022

SAIC

The molecular mechanisms that control adipocyte behaviorin breast cancer (BrCA) context remain unclear.We previously reported that the expression of RAC3coactivator in adipose tissue (AT) adjacent to tumorsfrom BrCA patients, was high in 59% of the samples,showing active NF-kB in nucleus and elevated levels ofpro-inflammatory cytokines (TNF and MCP1). Moreover,3T3-L1 adipocytes (3T3-L1ad) exposed to conditionedmedium (CM) from T-47D BrCA cells, exhibited higherRAC3 levels compared to CM from other tumoral andnon-tumoral cells. Therefore, the aim of this work was toelucidate the role of RAC3 and the mechanism by whichit is modulated in BrCA-associated adipocytes. First, weevaluated TNF and MCP1 levels by dot plot and qPCR,respectively, in 3T3-L1ad stimulated with T-47D CM orserum-free medium. Both molecules showed higher levelswith T-47D CM (p