BACKGROUND: Breast cancer (BC) is the most common type of cancer affecting women, and it is characterized by a high rate of proliferation of mutated breast cells, and its subtypes differ in their aggressive phenotype and prognosis. In this context, breast cancer aggressiveness may be related to the activation of inflammatory pathways, such as the Tumor Necrosis Factor Alpha (TNF-α) pathway, which regulates cell survival and cancer progression. Soluble TNF-α (sTNF-α) binds to Tumor Necrosis Factor Receptor 1 (TNFR1) and activates pathway members, such as JUN, which is linked to the regulation of apoptosis. AIM: This study aims to evaluate the expression of TNF and pathway members at the mRNA level through in silico and in vitro analyses. METHODOLOGY: The XENA platform was used to analyze the expression of TNF and pathway members at the mRNA level, using the TCGA-BRCA, TCGA target GTEx, and BC Cell Lines (Heiser, 2012) databases. Genes were analyzed individually and as a signature. RT-qPCR was performed to quantify the mRNA levels of TNF and pathway members in non-tumoral  and tumor breast cell lines. RESULTS: In silico analysis showed that the signature composed of TNF and pathway members had highest expression in tumor tissue and in the most aggressive subtype, known as basal subtype. In the individual gene analysis, TNF was also most expressed in the basal subtype and tumor tissue, while JUN and TNFR1 were most  expressed in normal tissue. In the cell lines analyzed in silico, the basal samples had highest JUN expression compared to the luminal samples. The in vitro RT-qPCR results with the cell lines showed no significant results. CONCLUSION: TNF-α is closely related to tumor progression, and the pathway members act together, being most expressed in the most aggressive subtype and in tumor tissue.