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miR-29a activates Hes1 by targeting Nfia in esophageal carcinoma cell line TE-1

MicroRNA (miR)-29a has been associated with carcinogenesis in humans; however, its functional significance in esophageal squamous cell carcinoma (ESCC) is yet to be determined. In the present study, the expression of miR-29a was markedly downregulated in ESCC tissue and the ESCC TE-1 cell line, comp...

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Detalles Bibliográficos
Autores principales: LIU, CHANG, DUAN, PING, LI, BO, HUANG, CHUNTIAN, JING, YING, YAN, WENHAI
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4246642/
https://www.ncbi.nlm.nih.gov/pubmed/25435940
http://dx.doi.org/10.3892/ol.2014.2678
Descripción
Sumario:MicroRNA (miR)-29a has been associated with carcinogenesis in humans; however, its functional significance in esophageal squamous cell carcinoma (ESCC) is yet to be determined. In the present study, the expression of miR-29a was markedly downregulated in ESCC tissue and the ESCC TE-1 cell line, compared with normal esophageal tissue and cells. Furthermore, the present study identified that the forced expression of miR-29a in TE-1 cells significantly reduced cell proliferation and migration. miR-29a overexpression did not affect the expression of Notch1, however, it did increase the gene expression levels of hairy and enhancer of split 1 (Hes1), which is the key effector of the Notch signaling pathway. Direct targeting by miR-29a resulted in the downregulation of nuclear factor 1 A (Nfia), which represses the transcriptional activity of the Hes1 promoter. Furthermore, knockdown of Nfia increased Hes1 expression and inhibited cell growth in TE-1 cells. These results indicate that a low level of miR-29a expression is involved in ESCC tumorigenesis, and exogenous expression of miR-29a may repress cancer cell growth by downregulating Nfia and activating the Notch signaling pathway.