Tristetraprolin (TTP) is an anti-inflammatory and tumor suppressor protein that induces the degradation of specific mRNAs. We and others have reported that TTP is down-regulated in invasive breast cancer (BC) compared with normal tissue. To better understand the role of this protein in BC development, we carried out an integrative analysis using data from The Cancer Genome Atlas, the Molecular Taxonomy of Breast Cancer International Consortium, the Clinical Proteomic Tumor Analysis Consortium, and samples from Hospital Curie BC patients. Using this information, we found that BCs display lower TTP expression than adjacent normal tissues. In addition, TTP levels were lower when the clinical stage of BC patients was higher, and reduced TTP expression was associated with poor prognosis in pre-menopausal women. Besides, we have determined a negative correlation between TTP and MKI67 expression in BC and their adjacent tissue, but not in normal breast samples. Finally, we found negative correlations between TTP levels and Ki-67 protein, tumor size as well as Cyclin D1 and TNFα mRNAs. These observations support the role of TTP as a tumor suppressor and anti-inflammatory protein in BC. Surprisingly, we not only found a positive correlation between TTP and the inflammatory cytokine IL6 mRNAs in all BC molecular subtypes but also in normal tissue. Moreover, TTP expression correlated positively with phosphorylated STAT3 (a transcription factor commonly activated by IL6) levels. Therefore, we postulated that IL6 induces TTP expression through STAT3 activation in mammary cells. Our results show that this cytokine induces TTP expression in luminal breast cancer cells in culture in a time-dependent manner. We propose that this signaling pathway is part of inflammation normal regulation, which remains active in breast cancer cells. We postulate that our results may support the reported paradoxical activities of IL6 and STAT3 in normal and tumor mammary cells.