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MicroRNA-26b suppresses autophagy in breast cancer cells by targeting DRAM1 mRNA, and is downregulated by irradiation

MicroRNAs (miRs) are small RNAs that do not code for proteins, but instead decrease the stability and suppress the translation of target mRNAs by binding with complementary sequences in their 3′-untranslated regions (3′-UTRs). In the present study, it is reported that breast cancer tumor tissue, as...

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Detalles Bibliográficos
Autores principales: Meng, Cuida, Liu, Yang, Shen, Yannan, Liu, Shuchun, Wang, Zhicheng, Ye, Qingsheng, Liu, Hongyang, Liu, Xiaodong, Jia, Lili
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5774516/
https://www.ncbi.nlm.nih.gov/pubmed/29399189
http://dx.doi.org/10.3892/ol.2017.7452
Descripción
Sumario:MicroRNAs (miRs) are small RNAs that do not code for proteins, but instead decrease the stability and suppress the translation of target mRNAs by binding with complementary sequences in their 3′-untranslated regions (3′-UTRs). In the present study, it is reported that breast cancer tumor tissue, as well as irradiated MCF7 breast cancer cells, exhibit decreased levels of miR-26b expression compared with normal breast tissue and MCF7 cells without exposure to radiation. Additionally, a luciferase reporter assay was used to demonstrate that miR-26b directly targetsDNA damage-regulated autophagy modulator 1 (DRAM1). MCF7 cells that were transfected with an miR-26b mimicexhibited the downregulated expression of DRAM1 protein and a reduced level of irradiation-induced autophagy. Inhibiting miR-26b resulted in the upregulation of DRAM1 and increased levels of irradiation-induced autophagy in MCF7 cells. These results suggest that therapeutic strategies to target miR-26b may increase the efficacy of certain types of cancer therapy.