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MicroRNA-495 induces breast cancer cell migration by targeting JAM-A

MicroRNAs (miRNAs) are small, non-coding RNAs that function as post-transcriptional regulators of gene expression. The deregulated expression of miRNAs is associated with a variety of diseases, including breast cancer. In the present study, we found that miR-495 was markedly up-regulated in clinical...

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Detalles Bibliográficos
Autores principales: Cao, Minghui, Nie, Weiwei, Li, Jing, Zhang, Yujing, Yan, Xin, Guan, Xiaoxiang, Chen, Xi, Zen, Ke, Zhang, Chen-yu, Jiang, Xiaohong, Hou, Dongxia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Higher Education Press 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4225486/
https://www.ncbi.nlm.nih.gov/pubmed/25070379
http://dx.doi.org/10.1007/s13238-014-0088-2
Descripción
Sumario:MicroRNAs (miRNAs) are small, non-coding RNAs that function as post-transcriptional regulators of gene expression. The deregulated expression of miRNAs is associated with a variety of diseases, including breast cancer. In the present study, we found that miR-495 was markedly up-regulated in clinical breast cancer samples by quantitative real time-PCR (qRT-PCR). Junctional adhesion molecule A (JAM-A) was predicted to be a potential target of miR-495 by bioinformatics analysis and was subsequently verified by luciferase assay and Western blotting. JAM-A was found to be negatively correlated with the migration of breast cancer cells through loss-of-function and gain-of-function assays, and the inhibition of JAM-A by miR-495 promoted the migration of MCF-7 and MDA-MB-231 cells. Furthermore, overexpression of JAM-A could restore miR-495-induced breast cancer cell migration. Taken together, our findings suggest that miR-495 could facilitate breast cancer progression through the repression of JAM-A, making this miRNA a potential therapeutic target. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s13238-014-0088-2) contains supplementary material, which is available to authorized users.