Tumor Heterogeneity in Triple-Negative Breast Cancer: Shedding Light on the Role of AKT and RUNX

Abstract

Breast cancer remains a significant health challenge worldwide, characterized byits diverse subtypes and varying prognoses. Among these, triple-negative breastcancer (TNBC) is particularly aggressive and lacks targeted therapies due to theabsence of estrogen receptors, progesterone receptors, and HER2 expression. Theheterogeneity of tumors in the TNBC subtype complicates treatment strategies, asdiverse cellular subpopulations exhibit different molecular characteristics andresponses to therapy. Key signaling pathways, such as the AKT pathway, playcritical roles in the progression and survival of TNBC cells. Similarly, the RUNXfamily of transcription factors has emerged as an influential player in TNBC,regulating genes involved in cell proliferation, differentiation, and apoptosis.Recent studies highlight the intricate cross-talk between the AKT pathway andthe transcriptional activity of different isoforms of RUNX, which may contributeto the aggressive nature of TNBC. Understanding this interaction provides newinsights into potential therapeutic targets, offering hope for more effective treatments for patients with this challenging breast cancer subtype. This reviewexplores the complex tumor heterogeneity in TNBC, the fundamental roles ofAKT and RUNX, and their interaction, with the aim of illuminating new avenuesfor interdisciplinary intervention and improving clinical outcomes in breastcancer in general and TNBC in particular.