Suppressive and Hypermethylated MicroRNAs in the Pathogenesis of Breast Cancer


如何引用文章

全文:

开放存取 开放存取
受限制的访问 ##reader.subscriptionAccessGranted##
受限制的访问 订阅存取

详细

MicroRNAs (miRNAs) are involved in oncogenesis by suppression of proto-oncogenes or tumor suppressive genes. This review presents data of suppressive miRNAs role in the mechanisms of occurrence and development of malignant tumors of breast cancer as the example—that is the most widespread oncopathology in women. Targets and functions of suppressive and antimetastatic miRNAs have been illustrated, as well as for suppressive miRNAs with an oncogenic potential (such as miR-200a, miR-200c) that appears probably owing to the ability of miRNA to interact with a variety of targets depending on the cellular content. Based on the published and the authors’ own data, the role of hypermethylation of promoter regions in inhibition of expression and regulatory function of miRNA genes in breast cancer was characterized. In conclusion, the authors pointed future prospects of clinical application of suppressive miRNAs in diagnostics and treatment of breast cancer.

作者简介

V. Loginov

Institute of General Pathology and Pathophysiology; Research Center of Medical Genetics

Email: burdennyy@gmail.com
俄罗斯联邦, Moscow, 125315; Moscow, 115478

E. Filippova

Institute of General Pathology and Pathophysiology

Email: burdennyy@gmail.com
俄罗斯联邦, Moscow, 125315

S. Kurevlev

Institute of General Pathology and Pathophysiology

Email: burdennyy@gmail.com
俄罗斯联邦, Moscow, 125315

M. Fridman

Institute of General Genetics

Email: burdennyy@gmail.com
俄罗斯联邦, Moscow, 117971

A. Burdennyy

Institute of General Pathology and Pathophysiology; Emanuel Institute of Biochemical Physics

编辑信件的主要联系方式.
Email: burdennyy@gmail.com
俄罗斯联邦, Moscow, 125315; Moscow, 119334

E. Braga

Institute of General Pathology and Pathophysiology; Research Center of Medical Genetics; Emanuel Institute of Biochemical Physics

Email: burdennyy@gmail.com
俄罗斯联邦, Moscow, 125315; Moscow, 115478; Moscow, 119334


版权所有 © Pleiades Publishing, Inc., 2018
##common.cookie##