摘要
富含半胱氨酸运动神经元蛋白1 (CRIM1),是一种新型的骨形成蛋白(BMPs)拮抗剂,报道称其能调节BMPs前体蛋白成熟并能转运BMPs到细胞表面。先前的研究已经表明,CRIM1是调节胎盘发育、器官形成、血管生成、肾脏病的重要参与者。本文,我们提出CRIM1是癌症恶化和转移的潜在危险因素。上皮细胞间质转型(EMT)以失去上皮表型并获得间质特性为特征,与肿瘤的侵袭和转移关系密切;同时,我们不能忽视血管形成在癌症发生和恶化中的重要性。在这个综述中,我们总结了CRIM1的结构特征和前期研究。此外,由于CRIM1在上皮细胞间质转型(EMT),毛细血管形成和血管生成和稳定的潜在作用,它可能与肿瘤的发生和恶化相关,我们首次推测其可能是癌症相关因子。
关键词: 拮抗剂,血管生成,骨形成蛋白,癌症治疗的目标,富含半胱氨酸运动神经元蛋白1,上皮细胞间质转型。
Current Cancer Drug Targets
Title:CRIM1, the Antagonist of BMPs, is a Potential Risk Factor of Cancer
Volume: 14 Issue: 7
Author(s): Hui Zeng and Liling Tang
Affiliation:
关键词: 拮抗剂,血管生成,骨形成蛋白,癌症治疗的目标,富含半胱氨酸运动神经元蛋白1,上皮细胞间质转型。
摘要: Cysteine-rich motor neuron1 protein (CRIM1), a novel antagonist of bone morphogenetic proteins (BMPs), is reported to regulate the processing of BMPs preprotein into mature protein and the delivery of BMPs to the cell surface. Previous studies have shown that CRIM1 is an important player in regulating placental development, organogenesis, angiogenesis and kidney disease. Here, we propose that CRIM1 is a potential risk factor in cancer progression and metastasis. The epithelial-mesenchymal transition (EMT), which is characterized by the loss of epithelial phenotype and the acquisition of mesenchymal characteristics, is closely associated with invasion and metastasis of tumors. At the same time, it is hard for us to ignore the importance of angiogenesis in the genesis and progression of cancer. In this review we summarized the construction and previous researches of CRIM1. Furthermore, as it may be involved in tumor development and progression through its potential role in the EMT, capillary formation and angiogenesis maintenance, we proposed for the first time that CRIM1 may be a cancer related factor.
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Cite this article as:
Zeng Hui and Tang Liling, CRIM1, the Antagonist of BMPs, is a Potential Risk Factor of Cancer, Current Cancer Drug Targets 2014; 14 (7) . https://dx.doi.org/10.2174/1568009614666140725094125
DOI https://dx.doi.org/10.2174/1568009614666140725094125 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
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