MicroRNA-21 promotes the cell proliferation, invasion and migration abilities in ovarian epithelial carcinomas through inhibiting the expression of PTEN protein

MicroRNA-21 promotes the cell proliferation, invasion and migration abilities in ovarian epithelial carcinomas through inhibiting the expression of PTEN protein
复制标题

DOI:
10.3892/ijmm_00000530
复制
发表时间:
2010-12-01
影响因子:
5.4
通讯作者:
Huang, Yu
Huang, Yu
中科院分区:
医学3区
文献类型:
--
作者:
Lou, Yanhui;Yang, Xingsheng;Huang, Yu

文献摘要

被引文献

相似文献

卵巢癌,特别是占卵巢癌90%的上皮性卵巢癌(EOC),仍然是妇科恶性肿瘤中死亡的主要原因。然而,与其恶性生物学行为相关的因素仍然知之甚少。越来越多的证据表明,microRNAs(miRNAs)在肿瘤的发生、发展中起着重要的作用,它调控着多种生物学过程。miR-21在各种肿瘤中经常被观察到异常过表达。使用实时PCR,我们证实miR-21在人EOC组织和细胞系中显著过表达。miR-21的过表达与组织分化、临床病理分期和淋巴结转移相关,我们发现通过抑制剂敲低miR-21可导致细胞增殖显著降低,细胞迁移和侵袭能力降低。此外,我们证明了miR-21的敲低显著增加了卵巢癌中已知的肿瘤抑制因子PTEN的表达。总的来说,我们的研究结果表明,miR-21可能通过调节PTEN在EOC的启动和进展中起重要作用。
Ovarian cancer, especially epithelial ovarian cancer (EOC), which accounts for 90% of ovarian cancer, continues to be the leading cause of death among gynecological malignancies. However, the factors associated with its malignant biological behavior are still poorly understood. Accumulating evidence suggests that microRNAs (miRNAs), regulating diverse biological processes, may play an important role in tumorigenesis and development. miR-21 has been frequently observed to be aberrantly overexpressed in various tumors. Using real-time PCR, we confirmed that miR-21 was significantly overexpressed in human EOC tissues and cell lines. The overexpression of miR-21 correlated with histological differentiation, clinicopathological stage, and lymph node metastasis, and we showed that knockdown of miR-21 by an inhibitor caused a significant reduction in cell proliferation and decrease in cell migration and invasion abilities. Furthermore, we demon-strated that knockdown of miR-21 significantly increased the expression of PTEN, a known tumor suppressor in ovarian cancer. Collectively, our findings suggest miR-21 may be important in the initiation and progression of EOC as an oncomiR, likely through regulating PTEN.