Breast cancer, notably Triple-negative breast cancer (TNBC), a subtype lacking expression of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor II (HER2), remains a significant global health issue due to its poor prognosis and high invasiveness. This study investigates oleanolic acid (OA), a compound that exhibits a broad spectrum of biological activities, such as anti-inflammatory, hepatoprotective, analgesic, cardiotonic, sedative, and anticancer properties. Numerous investigations have explored the potential health advantages of OA derived from natural sources, identifying it as a promising candidate for the development of novel preventative and therapeutic agents for various ailments. Additionally, the abundance of OA in plant-based foods renders it an appealing target for dietary interventions and the development of functional foods. However, the anti-cancer profile of OA against TNBC cells has not been fully elucidated. We discovered that OA could inhibit TNBC MDA-MB-231 cell proliferation and induce cell cycle arrest. OA's effect is realized through the downregulation of cyclin D1, CDK4, and p-cdc25c activities, analyzed via methylene blue assay, flow cytometry, and Western Blot. Moreover, OA was found to disrupt EGFR/Ras/ PI3K/ AKT/mTOR and EGFR/ERK1/2/GSK-3β pathways, thereby modulating cell cycle checkpoint proteins p53 and p21Cip1/Waf1. We also noted OA's ability to counteract EGF-induced protein upregulation and to promote cell cycle checkpoint proteins. Our study further elucidates the pro-apoptotic role of OA. The compound's apoptotic influence, marked by increased BAD and cytochrome c expression, was observed under various dosages. OA also induced a decrease in ATP production, signifying a metabolic shift, and downregulated mitochondrial-associated BCL-2 family proteins, potentially affecting apoptosis initiation markers. OA additionally modulated key apoptotic and cell cycle regulators in an EGF-stimulated cell model, leading to upregulated expressions of p21Cip1/Waf1, p53, caspase-9 and caspase-3, and a decrease in p-JNK expression. Lastly, our investigation into OA's anti-metastatic properties reveals its ability to downregulate matrix metalloproteinases MMP-2 and MMP-9, decrease the activity of released MMP-2 by modified zymography, and the reduced expression of migration marker VEGF, regulated by the c-Jun transcription factor. These findings suggest that OA's inhibitory effect on metastasis occurs via EGFR/p38 MAPK/JAK3/STAT-3, EGFR/ERK/STAT-3, and EGFR/JNK/c-Jun signaling pathways. Results of this study illuminate OA's potential therapeutic benefits in managing TNBC proliferation, apoptosis, and metastasis, thereby offering a promising avenue for the development of more effective treatment strategies from the perspective of diet and cancer.