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miR-34a suppresses proliferation and induces apoptosis of human lens epithelial cells by targeting E2F3

microRNA (miRNA) is abnormally expressed in numerous diseases, and it was intimately associated with cell proliferation and apoptosis. However, the mechanism by which miRNAs control cataractogenesis remains unclear. In the current study, it was demonstrated that miR-34a was highly expressed in the c...

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Detalles Bibliográficos
Autores principales: Xiang, Wu, Lin, Haotian, Wang, Qilin, Chen, Wan, Liu, Zhaochuan, Chen, Hui, Zhang, Hui, Chen, Weirong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5355663/
https://www.ncbi.nlm.nih.gov/pubmed/27840975
http://dx.doi.org/10.3892/mmr.2016.5901
Descripción
Sumario:microRNA (miRNA) is abnormally expressed in numerous diseases, and it was intimately associated with cell proliferation and apoptosis. However, the mechanism by which miRNAs control cataractogenesis remains unclear. In the current study, it was demonstrated that miR-34a was highly expressed in the cataractous lens by stem-loop reverse transcription-quantitative polymerase chain reaction. Trying to investigate the role of miR-34a in human lens epithelial cells, miR-34a mimics were transfected into SRA01/04 cells, and this suppressed proliferation and induced apoptosis. Subsequently, E2F3 was confirmed as a direct target of miR-34a. Downregulation of E2F3 by small interfering (si) RNA siE2F3 resulted in proliferation inhibition and apoptosis of SRA01/04 cells. Furthermore, it was demonstrated that miR-34a and siE2F3 downregulated E2F3 expression at a protein level. In summary, the current study demonstrated that miR-34a suppressed the proliferation and induced apoptosis of SRA01/04 cells by downregulating E2F3. These observations provide novel insights with potential therapeutic applications for the treatment of cataracts.