The Role of SLC7A11 in Cancer: Friend or Foe?

SIMPLE SUMMARY: Strikingly, there are many literature reports confirming that the SLC7A11 gene is closely related to the tumourigenesis, survival, proliferation, metastasis, therapeutic resistance, and other aspects of tumour cells. Meanwhile, the role of SLC7A11 in tumours is highly complex, and its pro-tumour and antitumour activities are obviously different. We summarised the biological characteristics of SLC7A11, including its structure, expression, function, regulation, and therapeutic approaches, and focused on the discussion and analysis of the possibility of SLC7A11 as a potential antitumour target, providing a theoretical basis for drug research and clinical tumour treatment. ABSTRACT: SLC7A11 controls the uptake of extracellular cystine in exchange for glutamate at a ratio of 1:1, and it is overexpressed in a variety of tumours. Accumulating evidence has shown that the expression of SLC7A11 is fine-tuned at multiple levels, and plays diverse functional and pharmacological roles in tumours, such as cellular redox homeostasis, cell growth and death, and cell metabolism. Many reports have suggested that the inhibition of SLC7A11 expression and activity is favourable for tumour therapy; thus, SLC7A11 is regarded as a potential therapeutic target. However, emerging evidence also suggests that on some occasions, the inhibition of SLC7A11 is beneficial to the survival of cancer cells, and confers the development of drug resistance. In this review, we first briefly introduce the biological properties of SLC7A11, including its structure and physiological functions, and further summarise its regulatory network and potential regulators. Then, focusing on its role in cancer, we describe the relationships of SLC7A11 with tumourigenesis, survival, proliferation, metastasis, and therapeutic resistance in more detail. Finally, since SLC7A11 has been linked to cancer through multiple approaches, we propose that its contribution and regulatory mechanism require further elucidation. Thus, more personalised therapeutic strategies should be adapted when targeting SLC7A11.