ERs) and progesterone receptors (PRs), as well as human epidermal growth factor receptor 2 (HER2). It is the most aggressive subtype of breast cancer, affecting about 15-20% of total breast cancer cases. Compared with other subtypes, TNBC tumors are associated with higher histologic grade and larger tumor size (1, 2). The current standard regimen for TNBC patients is a combination of surgery and chemotherapy (3), which often fails to effectively slow down the tumor progression. Hence, TNBC patients have lower overall survival (81% vs. 91%) and disease-free survival (72% vs. 86%) compared with non-TNBC patients (4). Given the lack of ER and HER2 in this subtype, there is no molecular characterization that allows this subtype to be targeted. Uncontrolled proliferation of cancer cells is metabolically demanding. The metabolic pathways utilized by cancer cells to sustain high-energy demands and biosynthesis differ from those employed by healthy cells (5). Challenged by hostile environments such as hypoxia and acute interruptions in nutrient availability, cancer cells typically develop metabolic plasticity, which enables the utilization of available nutrients as bioenergetic substrates. This metabolic flexibility allows maintained ATP production under varying physiological and pathological conditions and is primarily regulated by substrate concentration, hormone levels, blood flow, oxygen supply, and workload (6). Cancer-associated changes in cellular metabolism may also be a direct consequence of oncogenic signal transduction.

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