摘要
黑素瘤优先表达抗原(PRAME)是富含亮氨酸重复(LRR)蛋白的PRAME家族最具有特征的成员之一。哺乳动物的基因组中包含有PRAME家族的多个成员而在其他脊椎动物基因组中只确定有一个像PRAME的LRR蛋白。PRAME基因是一种肿瘤/睾丸抗原,除睾丸外正常成人组织的表达水平非常低,但在多种肿瘤细胞中有高水平表达。与其他大多数肿瘤/睾丸抗原对照,不仅在实体瘤有PRAME的表达,也在白血病细胞中有表达。PRAME和PRAME基因家族的其他成员表达受表观遗传的调控。PRAME与不同途径的相互作用,可能直接参与了癌细胞的恶性表型。例如,PRAME能够主要抑制这些细胞中视黄酸的信号转导。另一方面, PRAME衍生肽是被细胞毒性T细胞识别的抗原表位,在免疫治疗策略里PRAME可代表一个有吸引力的靶点。
关键词: 癌/睾丸抗原,黑色素瘤的优先表达抗原,视黄酸信号,DNA甲基化,霍奇金淋巴瘤。
Current Cancer Drug Targets
Title:Preferentially Expressed Antigen in Melanoma (PRAME) and the PRAME Family of Leucine-Rich Repeat Proteins
Volume: 16 Issue: 5
Author(s): Nora Hermes, Stefanie Kewitz, Martin S. Staege
Affiliation:
关键词: 癌/睾丸抗原,黑色素瘤的优先表达抗原,视黄酸信号,DNA甲基化,霍奇金淋巴瘤。
摘要: Preferentially expressed antigen in melanoma (PRAME) is the best characterized member of the PRAME family of leucine-rich repeat (LRR) proteins. Mammalian genomes contain multiple members of the PRAME family whereas in other vertebrate genomes only one PRAME-like LRR protein was identified. PRAME is a cancer/testis antigen that is expressed at very low levels in normal adult tissues except testis but at high levels in a variety of cancer cells. In contrast to most other cancer/testis antigens, PRAME is expressed not only in solid tumors but also in leukemia cells. Expression of PRAME and other members of the PRAME family is regulated epigenetically. PRAME interacts with varying pathways that might be directly involved in the malignant phenotype of cancer cells. For instance, PRAME is able to dominantly repress retinoic acid signaling in these cells. On the other hand, PRAME-derived peptides can be recognized as epitopes by cytotoxic T cells and PRAME represents an attractive target for immunological treatment strategies.
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Cite this article as:
Nora Hermes, Stefanie Kewitz, Martin S. Staege , Preferentially Expressed Antigen in Melanoma (PRAME) and the PRAME Family of Leucine-Rich Repeat Proteins, Current Cancer Drug Targets 2016; 16 (5) . https://dx.doi.org/10.2174/1568009616666151222151818
DOI https://dx.doi.org/10.2174/1568009616666151222151818 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
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