miR⁃143与骨肉瘤发生、进展及预后关系的研究进展  被引量:2

Research progress of the relationship between miR⁃143 and the occurrence,progression and prognosis of osteosarcoma

在线阅读下载全文

作  者:刘加明 徐红[1] 杨坤[1] 向阳[1] LIU Jiaming;XU Hong;YANG Kun;XIANG Yang(Guizhou Medical University,Guiyang,Guizhou,China,550001)

机构地区:[1]贵州医科大学,贵州贵阳550001

出  处:《分子诊断与治疗杂志》2022年第5期719-722,共4页Journal of Molecular Diagnostics and Therapy

基  金:贵州省科技计划项目(黔科合LH字[2017]7176号)。

摘  要:骨肉瘤是威胁人类生命安全的恶性疾病,近年来发病率呈逐渐上升趋势。随着医疗技术的不断进步与发展,骨肉瘤患者远期生存率得以大大提升,但化疗抵抗、肿瘤转移仍是导致患者预后不良的危险因素。目前,关于微RNA(miRNA)与骨肉瘤关系的报道逐渐增多,多数研究表明,骨肉瘤miRNA表达与其发病具有密切联系。其中miRNA⁃143(miR⁃143)可能作为抑癌基因参与了骨肉瘤发生、发展。骨肉瘤发病与体内miR⁃143水平下降有关,且骨肉瘤细胞增殖、侵袭及转移能力会随着miR⁃143水平上升而发生改变。本文主要对miR⁃143所调控的基因(PAI⁃1、MMPs、K⁃ras等)与骨肉瘤发生、发展及预后之间的关系进行阐述。Objective Osteosarcoma is a malignant disease that threatens human life,and its incidence has been on the rise in recent years.With the continuous progress and development of medical technology,the long⁃term survival rate of patients with osteosarcoma has greatly improved,but chemotherapy resistance and tumor metastasis are still the risk factors leading to poor prognosis of patients.At present,reports on the relationship between microRNA(miRNA)and osteosarcoma are increasing,and most studies have shown that the expression of miRNA in osteosarcoma is closely related to its pathogenesis.Among them,miRNA⁃143(miR⁃143)may be involved in the occurrence and development of osteosarcoma as a tumor suppressor gene.The pathogenesis of osteosarcoma is related to the decreasing of miR⁃143 level in vivo,and the proliferation,invasion and metastasis ability of osteosarcoma cells will change with the increase of miR⁃143 level.This article describes the relationship between the genes regulated by miR⁃143(PAI⁃1,MMPs,K⁃ras,etc.),and the occurrence,development,and prognosis of osteosarcoma.

关 键 词:骨肉瘤 miR⁃143 增殖 侵袭与转移 预后 

分 类 号:R738.1[医药卫生—肿瘤]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象