首页> 外文期刊>Life sciences >The multiple regulation of metastasis suppressor NM23-H1 in cancer
【24h】

The multiple regulation of metastasis suppressor NM23-H1 in cancer

机译:癌症中转移抑制作用NM23-H1的多种调节

获取原文
获取原文并翻译 | 示例
           

摘要

Metastasis is one of the leading causes of mortality in cancer patients. As the firstly identified metastasis suppressor, NM23-H1 has been endowed with expectation as a potent target in metastatic cancer therapy during the past decades. However, many challenges impede its clinical use. Accumulating evidence shows that NM23-H1 has a dichotomous role in tumor metastasis as a suppressor and promoter. It has potentially attributed to its versatile biochemical characteristics such as nucleoside diphosphate kinase (NDPK) activity, histidine kinase activity (HPK), exonuclease activity, and protein scaffold, which further augment the complexity and uncertainty of its physiological function. Simultaneously, tumor cells have evolved multiple ways to regulate the expression and function of NM23-H1 during tumorigenesis and metastasis. This review summarized and discussed the regulatory mechanisms of NM23-H1 in cancer including transcriptional activation, subcellular location, enzymatic activity, and protein degradation, which significantly modulate its anti-metastatic function.
机译:转移是癌症患者死亡的主要原因之一。作为最早发现的转移抑制因子,NM23-H1在过去几十年中被认为是转移癌治疗的有效靶点。然而,许多挑战阻碍了其临床应用。越来越多的证据表明,NM23-H1在肿瘤转移中作为抑制子和启动子起着二分法的作用。它具有多种生物化学特性,如核苷二磷酸激酶(NDPK)活性、组氨酸激酶(HPK)、核酸外切酶活性和蛋白质支架,进一步增加了其生理功能的复杂性和不确定性。同时,在肿瘤发生和转移过程中,肿瘤细胞通过多种方式调节NM23-H1的表达和功能。本文综述并讨论了NM23-H1在肿瘤中的调节机制,包括转录激活、亚细胞定位、酶活性和蛋白质降解,这些机制显著调节其抗转移功能。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号