Breast cancer arises from the malignant transformation of mammary epithelial cells under the influence of various carcinogenic factors, leading to a gradual increase in its prevalence. This disease has become the leading cause of mortality among female
malignancies, posing a significant threat to the health of women. The timely identification of
breast cancer remains challenging, often resulting in diagnosis at the advanced stages of the disease. Conventional therapeutic approaches, such as surgical excision,
chemotherapy and
radiotherapy, exhibit limited efficacy in controlling the progression and
metastasis of the disease. Regulated cell death (RCD), a process essential for physiological tissue cell renewal, occurs within the body independently of external influences. In the context of
cancer, research on RCD primarily focuses on cuproptosis, ferroptosis and pyroptosis. Mounting evidence suggests a marked association between these specific forms of RCD, and the onset and progression of
breast cancer. For example, a cuproptosis vector can effectively bind
copper ions to induce cuproptosis in
breast cancer cells, thereby hindering their proliferation. Additionally, the expression of ferroptosis‑related genes can enhance the sensitivity of
breast cancer cells to
chemotherapy. Likewise, pyroptosis‑related
proteins not only participate in pyroptosis, but also regulate the tumor microenvironment, ultimately leading to the death of
breast cancer cells. The present review discusses the unique regulatory mechanisms of cuproptosis, ferroptosis and pyroptosis in
breast cancer, and the mechanisms through which they are affected by conventional
cancer drugs. Furthermore, it provides a comprehensive overview of the significance of these forms of RCD in modulating the efficacy of
chemotherapy and highlights their shared characteristics. This knowledge may provide novel avenues for both clinical interventions and fundamental research in the context of
breast cancer.