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. 2018 May 15;9(37):24871. doi: 10.18632/oncotarget.25461

Correction: MiR-124 acts as a target for Alzheimer’s disease by regulating BACE1

Fengmao An 1,2,*, Guohua Gong 1,2,3,*, Yu Wang 1,2, Ming Bian 1,2, Lijun Yu 1,2, Chengxi Wei 1,2
PMCID: PMC5973865  PMID: 29873327

This article has been corrected: The correct Materials and Methods and Figure 2 are given below: The authors declare that these corrections do not change the results or conclusions of this paper.

Figure 2.

Figure 2

(A) MTT assay results showed that Aβ inhibited the viability of SH-SY5Y cells and downregulation of BACE1 enhanced the inhibitory effects of Aβ; (B) downregulation of miR-124 relieved Aβ-induced viability inhibition of SH-SY5Y cells; (C) flow cytometric analysis results showed that Aβ-induced apoptosis of SH-SY5Y cells and downregulation of BACE1 enhanced the induced effects of Aβ; (D) downregulation of miR-124 decreased apoptosis of SH-SY5Y cells in the presence of Aβ.

Luciferase reporting assay

The 3’ UTR of BACE1 and the CMV promoter were amplified from human chromosomal DNA and pcDNA3.1 (+) and cloned into the pGL3-luciferase basic vector (Promega, Madison, WI, USA). Sequences of primers and cloning strategy are available on request. For the luciferase assays, 50 nM of miR-124 mimics or scrambled RNA were co-transfected with the reporter vector and the Renilla control vector (Promega, Madison, WI, USA) into the HEK293 cells by Lipofectamine 2000 (Invitrogen, Carlsbad, CA, USA). 24 h post transfection, the measurements were performed using the Dual luciferase re-porter assay kit (Promega, Madison, WI, USA). Or the HEK293 cells post the transfection for 24 h was lyzed for western blot analysis.

Original article: Oncotarget. 2017; 8:114065-114071. https://doi.org/10.18632/oncotarget.23119


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