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.
摘要：
SLC7A11以1：1的比例控制细胞外胱氨酸的摄取以交换谷氨酸，并且在多种肿瘤中过表达。越来越多的证据表明，SLC7A11的表达在多个水平上被微调，并在肿瘤中发挥不同的功能和药理作用，如细胞氧化还原稳态，细胞生长和死亡，和细胞代谢。许多报道表明，抑制SLC7A11的表达和活性有利于肿瘤治疗；因此，SLC7A11被认为是一个潜在的治疗靶点。然而,新出现的证据还表明，在某些情况下，抑制SLC7A11有利于癌细胞的存活,并赋予耐药性的发展。在这次审查中,首先简要介绍了SLC7A11的生物学特性,包括其结构和生理功能,并进一步总结其监管网络和潜在监管机构。然后，专注于它在癌症中的作用，我们描述了SLC7A11与肿瘤发生的关系，生存,扩散,转移,和更详细的治疗抗性。最后,由于SLC7A11通过多种方法与癌症有关，我们建议其贡献和监管机制需要进一步阐明。因此，针对SLC7A11时，应采用更个性化的治疗策略。
