SLC7A11 Inhibitors Represent a Promising Therapeutic Target by Facilitating the Induction of Ferroptosis in Breast Cancer.

Abstract

It is predicted with near certainty that an estimated 310,720 women will be diagnosed with invasive breast carcinoma in 2024, while the number of men will be significantly lower at around 2,800, highlighting the alarming prevalence of this cancer across the sexes. The Solute Carrier Family 7 Member 11(SLC7A11) gene is vital for the exchange of extracellular cystine for glutamate at a 1:1 ratio and its expression is significantly increased in various tumors. Numerous research studies have shown that SLC7A11 expression is fine-tuned at several levels, contributing to its pharmacological functions in tumors, such as maintaining cellular redox balance, promoting cell proliferation, and influencing ferroptosis. Many studies suggest that reducing SLC7A11 expression and activity may be beneficial for cancer treatment, making it a promising target for therapy. However, recent findings also suggest that inhibiting SLC7A11 in certain scenarios may increase the survival of cancer cells and promote drug resistance. This review begins with a brief overview of the properties of SLC7A11, including its structural features and physiological functions, followed by a summary of its potential regulators. We then delve deeper into its role in cancer, particularly breast cancer, and explore the relationships between SLC7A11 and ferroptosis, proliferation, metastasis, and therapeutic resistance. Consequently, more customized therapeutic approaches should be considered when targeting SLC7A11 in the context of breast cancer. Thus, high expression of SLC7A11 is associated with poor prognosis in breast cancer, and various inhibitors have been identified that can effectively target this transporter. Innovative therapeutic strategies, including immunotherapies targeting SLC7A11, can potentially reduce tumor growth and metastasis in breast cancer models.