Identification of miR-508-3p and miR-509-3p that are associated with cell invasion and migration and involved in the apoptosis of renal cell carcinoma

Identification of miR-508-3p and miR-509-3p that are associated with cell invasion and migration and involved in the apoptosis of renal cell carcinoma
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鉴定与细胞侵袭和迁移相关并参与肾细胞癌凋亡的miR-508-3p和miR-509-3p

DOI:
10.1016/j.bbrc.2012.02.060
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发表时间:
2012-03-23
影响因子:
3.1
通讯作者:
Lu, Ruijing
Lu, Ruijing
中科院分区:
生物学4区
文献类型:
--
作者:
Zhai, Qingna;Zhou, Liang;Lu, Ruijing

文献摘要

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microRNA(miRNAs)已经成为与人类癌症相关的多个过程的强大调节剂,包括细胞凋亡、增殖和迁移,这表明miRNA功能的调节在癌症进展中可能起关键作用。最近的研究发现,人血清/血浆中含有稳定表达的miRNA。如果它们被证明指示疾病状态,那么从外周血样本中测量的miRNA可能成为癌症常规临床检测的来源。我们的研究表明miR-508- 3 p和miR-509- 3 p在肾癌组织中表达下调。肾细胞癌(RCC)患者血浆中miR-508- 3 p而非miR-509- 3 p的水平显示出与对照血浆中的显著差异。此外,miR-508- 3 p和miR-509- 3 p过表达可抑制肾癌细胞(786-0)的增殖,诱导细胞凋亡,抑制细胞迁移。我们的数据表明,miR-508- 3 p和miR-509- 3 p作为肿瘤抑制基因在肿瘤形成过程中发挥了重要作用,它们可能成为RCC的新的诊断标志物。(C)2012 Elsevier Inc. All rights reserved.
MicroRNAs (miRNAs) have emerged as powerful regulators of multiple processes linked to human cancer, including cell apoptosis, proliferation and migration, suggesting that the regulation of miRNA function could play a critical role in cancer progression. Recent studies have found that human serum/plasma contains stably expressed miRNAs. If they prove indicative of disease states, miRNAs measured from peripheral blood samples may be a source for routine clinical detection of cancer. Our studies showed that both miR-508-3p and miR-509-3p were down-regulated in renal cancer tissues. The level of miR-508-3p but not miR-509-3p in renal cell carcinoma (RCC) patient plasma demonstrated significant differences from that in control plasma. In addition, the overexpression of miR-508-3p and miR-509-3p suppressed the proliferation of RCC cells (786-0), induced cell apoptosis and inhibited cell migration in vitro. Our data demonstrated that miR-508-3p and miR-509-3p played an important role as tumor suppressor genes during tumor formation and that they may serve as novel diagnostic markers for RCC. (C) 2012 Elsevier Inc. All rights reserved.