SLC7A11/xCT is a cystine/glutamate antiporter that imports cystine for glutathione (GSH) biosynthesis and antioxidant defense, and is overexpressed in many cancers. SLC7A11 overexpression promotes tumor growth by suppressing ferroptosis, a form of regulated cell death caused by lipid peroxidation. However, this also leads to glucose- and glutamine-dependent metabolism in SLC7A11-high cancer cells, creating metabolic vulnerabilities. This review summarizes SLC7A11's regulatory mechanisms in cancer, discusses its roles in promoting tumor development through ferroptosis-dependent and -independent functions, explores the mechanisms of SLC7A11-induced nutrient dependency, and proposes therapeutic strategies targeting SLC7A11. SLC7A11 is regulated by transcription factors like ATF4 and NRF2, epigenetic mechanisms, and post-translational modifications. It plays a critical role in suppressing ferroptosis by maintaining GSH levels, and its dysregulation can lead to ferroptosis resistance and tumor formation. SLC7A11 also promotes tumor development by enhancing drug, chemo-, and radio-resistance, and by facilitating nutrient dependency. The review highlights the importance of SLC7A11 in ferroptosis, nutrient dependency, and tumor biology, and suggests that targeting SLC7A11 could be a promising strategy for cancer therapy.SLC7A11/xCT is a cystine/glutamate antiporter that imports cystine for glutathione (GSH) biosynthesis and antioxidant defense, and is overexpressed in many cancers. SLC7A11 overexpression promotes tumor growth by suppressing ferroptosis, a form of regulated cell death caused by lipid peroxidation. However, this also leads to glucose- and glutamine-dependent metabolism in SLC7A11-high cancer cells, creating metabolic vulnerabilities. This review summarizes SLC7A11's regulatory mechanisms in cancer, discusses its roles in promoting tumor development through ferroptosis-dependent and -independent functions, explores the mechanisms of SLC7A11-induced nutrient dependency, and proposes therapeutic strategies targeting SLC7A11. SLC7A11 is regulated by transcription factors like ATF4 and NRF2, epigenetic mechanisms, and post-translational modifications. It plays a critical role in suppressing ferroptosis by maintaining GSH levels, and its dysregulation can lead to ferroptosis resistance and tumor formation. SLC7A11 also promotes tumor development by enhancing drug, chemo-, and radio-resistance, and by facilitating nutrient dependency. The review highlights the importance of SLC7A11 in ferroptosis, nutrient dependency, and tumor biology, and suggests that targeting SLC7A11 could be a promising strategy for cancer therapy.