Research Papers:

MiR-30a inhibits BECN1-mediated autophagy in diabetic cataract

Lu Zhang, Rong Cheng and Yusen Huang _

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Oncotarget. 2017; 8:77360-77368. https://doi.org/10.18632/oncotarget.20483

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Lu Zhang1,2, Rong Cheng2,3 and Yusen Huang2

1Department of Ophthalmology, School of Medicine, Shandong University, Jinan 250012, China

2Qingdao Eye Hospital, Shandong Eye Institute, Shandong Academy of Medical Sciences, Qingdao 266071, China

3College of Medicine, Qingdao University, Qingdao 266071, China

Correspondence to:

Yusen Huang, email: [email protected]

Keywords: miR-30a, BECN1, autophagy, diabetic cataract, lens epithelial cells

Received: May 07, 2017     Accepted: June 25, 2017     Published: August 24, 2017


Purpose: To investigate the role of microRNAs in the regulation of autophagy and apoptosis in lens epithelial cells (LECs) during diabetic cataract formation.

Methods: A miRNA microarray study and quantitative real-time PCR were performed to identify the expression of miRNAs in LECs of diabetic cataract. Human LECs were cultured in high glucose conditions as a diabetic cataract model. BECN1 and LC3B were detected by Western blotting and quantitative real-time PCR. The extent of apoptosis was measured using FACSCalibur flow cytometry.

Results: Downregulation of miR-30a was identified in LECs attached to diabetic cataract tissues. By the bioinformatic assay and the luciferase activity assay, BECN1 was found to be a direct target of miR-30a. MiR-30a reduced the BECN1-mediated autophagy activity induced by high glucose in LECs in vitro. The ratio of LECs apoptosis was also decreased.

Conclusion: MiR-30a was involved in the inhibition of autophagy by targeting BECN1 in LECs in human diabetic cataract.

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