The leading cause of mortality in patients with triple negative breast cancer (TNBC) is metastatic disease, due in large part to the absence of effective targeted therapies, reflecting substantial disease heterogeneity. Consequently, there is a critical need to identify novel molecular mechanisms that can be leveraged to suppress TNBC progression and improve patient survival. Tristetraprolin (TTP) is an RNA-binding protein that recognizes AU-rich elements (AREs) in the 3′ untranslated regions (UTRs) of select mRNAs and promotes their rapid degradation, including many encoding proteins that contribute to cancer-related processes. Loss of TTP expression has been correlated with more aggressive disease and reduced overall survival in patients, implicating TTP as a tumor suppressor across multiple cancer types, including breast cancer. To discover how TTP modulates tumorigenic phenotypes in advanced breast cancer, we generated stable cell lines expressing FLAG-tagged TTP in three highly aggressive and metastatic TNBC models. Transcriptomic profiling by RNA sequencing revealed that TTP broadly altered gene expression patterns across all three cell lines. Gene Set Enrichment Analysis (GSEA) further demonstrated that TTP significantly suppressed pathways involved in cell growth, metastasis, and stemness. Functional assays revealed that TTP robustly suppressed cell proliferation, stem cell frequency, migration, and invasiveness in vitro. Consistent with these findings, in vivo experiments showed that TTP expression significantly reduced tumor growth. We next sought to identify the mechanism underlying the anti-proliferative effect of TTP. Surprisingly, actinomycin D experiments demonstrated that TTP did not alter the decay kinetics of several well-characterized TTP target mRNAs, indicating that its tumor-suppressive activity in TNBC cells may occur independently of RNA destabilization. To directly test this, we engineered TNBC cell lines expressing an RNA-binding-deficient TTP mutant (C147R). Remarkably, this mutant recapitulated the suppression of all in vitro and in vivo tumor phenotypes observed with wild-type TTP. Together, these findings demonstrate that TTP exerts potent tumor-suppressive effects in TNBC cell models, inhibiting multiple oncogenic phenotypes and significantly attenuating tumor growth in vivo. Importantly, these effects occur through a mechanism that is independent of TTP’s canonical RNA-binding and RNA-destabilizing functions, revealing a previously unrecognized mode of TTP-mediated tumor suppression.