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. 2017 May 29;16(1):755–763. doi: 10.3892/mmr.2017.6640

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Copyright: © Chen et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 5. — miR-146a modulates apoptosis via the nuclear factor-κB signaling pathway. (A-C) SGC-7901 cells were transfected with an miR-146a mimic or inhibitor, or scrambled controls, at a final concentration of 10 nM. TAK1 was (D and E) knocked down or (F and G) overexpressed in SGC-7901 cells. Cells were subsequently analyzed for IκBα and Bcl-2 protein expression levels by western blotting. Blots were quantified by densitometry and normalized to β-actin. Data are representative of three independent experiments. *P<0.05; **P<0.01. miR, microRNA; TAK1, transforming growth factor β-activated kinase 1; IκBα, inhibitor of κBα; Bcl-2, B-cell lymphoma 2; si, small interfering; Ctrl, control.