Non-coding RNAs-regulated SLC7A11 modulates ferroptosis: a new strategy for cancer therapy.

Ferroptosis is an iron-dependent form of regulated cell death that plays a dual role in cancer progression and suppression. Solute carrier family 7 member 11 (SLC7A11/xCT) is a key regulator of tumor cell ferroptosis that promotes cystine uptake and glutathione synthesis. However, the regulatory mechanisms of ferroptosis remain unclear, which limits its application in cancer therapy. Recent studies have found that non-coding RNAs (ncRNAs), including lncRNAs, miRNAs, and circRNAs, participate in the process of ferroptosis by regulating SLC7A11. In this review, we summarize the mechanisms of ncRNAs that regulate SLC7A11 expression through transcriptional, post-transcriptional, and epigenetic ways to influence ferroptosis in tumor cells. Furthermore, we explore the potential use of the ncRNA/SLC7A11 axis as a therapeutic target for tumors, and introduce new strategies aimed at inducing ferroptosis and overcoming chemotherapy resistance, such as natural compounds targeting ncRNA and nano-delivery systems. This review will enhance our understanding of the potential of ncRNAs targeting SLC7A11 in tumor therapy and offer new approaches to investigating novel tumor diagnostic and therapeutic biochemical indicators in future clinical treatments.