The extrusion of anticancer drugs by members of the ATP-binding cassette (ABC) transporter family is one of the most widely recognized mechanisms of multidrug resistance, and can be considered a hijacking of their normal roles in the transport of xenobiotics, metabolites and signaling molecules across cell membranes. While roles in cancer multidrug resistance have been clearly demonstrated for P-glycoprotein (P-gp), Breast Cancer Resistance Protein (BCRP) and Multidrug Resistance Protein 1 (MRP1), direct evidence for a role in multidrug resistance in vivo is lacking for other family members. A less well understood but emerging theme is the drug efflux-independent contributions of ABC transporters to cancer biology, supported by a growing body of evidence that their loss or inhibition impacts on the malignant potential of cancer cells in vitro and in vivo. As with multidrug resistance, these contributions likely represent a hijacking of normal ABC transporter functions in the efflux of endogenous metabolites and signaling molecules, however they may expand the clinical relevance of ABC transporters beyond P-gp, BCRP and MRP1. This review summarizes established and emerging roles for ABC transporters in cancer, with a focus on neuroblastoma and ovarian cancer, and considers approaches to validate and better understand these roles.

ATP结合盒（ABC）转运蛋白家族成员对抗癌药物的挤压是最广泛认可的多药耐药性机制之一，可以认为是其在异源生物，代谢产物和信号分子转运中的正常作用被劫持跨细胞膜。尽管已明确证明P-糖蛋白（P-gp），乳腺癌抗性蛋白（BCRP）和多药抗性蛋白1（MRP1）在癌症多药抗性中的作用，但直接证据证明了体内多药抗性的作用其他家庭成员所缺少的。一个鲜为人知但新兴的主题是ABC转运蛋白对癌症生物学的独立于药物外排的作用，越来越多的证据表明它们的丢失或抑制作用会影响癌细胞在体外和体内的恶性潜能。与多药耐药一样，这些贡献可能代表了正常ABC转运蛋白在内源性代谢物和信号分子外流中的劫持，但它们可能将ABC转运蛋白的临床相关性扩展到P-gp，BCRP和MRP1之外。这篇综述总结了ABC转运蛋白在癌症中已确立和正在发挥的作用，重点是神经母细胞瘤和卵巢癌，并考虑了验证和更好地理解这些作用的方法。