HDAC7与肿瘤血管生成及其抗血管靶点治疗的研究进展
| 作者: |
1李希,
1陶光实
1 中南大学湘雅二医院妇产科，长沙 410000 |
| 通讯: |
李希
Email: lixi920815@126.com 陶光实 Email: taoguangshi@aliyun.com |
| DOI: | 10.3978/j.issn.2095-6959.2015.11.030 |
| 基金: | 2014 年度中华人民共和国人力资源和社会保障部出国留学人员重点资助课题 |
摘要
组蛋白脱乙酰基酶7(histone deacetylase7，HDAC7)属于Ⅱa类组蛋白脱乙酰基酶，是肿瘤血管生成的关键因子，研究表明HDAC7能影响血管内皮细胞的生长和增殖、改变血管内皮细胞的迁移能力，HDAC7与转录因子-肌细胞增强因子(myocyte enhancer factor2，MEF2)-2相互作用调节其下游靶基因基质金属蛋白酶(matrix metallo proteinase-10，MMP-10)-10，进而参与维持血管的完整性和稳定性，在实体瘤生长和转移中具有十分重要的作用，本文综述HDAC7与肿瘤血管新生的机制，以及该靶点在肿瘤血管靶点治疗中的研究进展。
关键词：
组蛋白去乙酰化酶
肌细胞增强因子
肿瘤血管
MMP-10
The progress of HDAC7 and tumor angiogenesis as a theraptic target
CorrespondingAuthor: LI Xi Email: lixi920815@126.com
DOI: 10.3978/j.issn.2095-6959.2015.11.030
Abstract
Histone deacetylase7 (HDAC7) ,which belongs to classⅡa HDACs, is a key factor of tumor angiogenesis. Researchers have reported that HDAC7 effected the growth and proliferation of vascular endothelial cell and changed the migratory capacity of endothelial cells. Interaction between HDAC7 and MEF2 (myocyte enhancer factor, MEF2) regulated its downstream target gene matrix metallo proteinase-10 (MMP-10), which played an important role in maintaining vascular stability and regulating angiogenesis, especially involving in the initiation and progression of solid tumors. We reviewed the mechanism of HDAC7 and its interaction withMEF2 in tumor angiogenesis, and proposed HDAC7 as an anti-angiogenesis target in tumor therapy.