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. 2020 Feb 13;21(4):1761–1770. doi: 10.3892/mmr.2020.10987

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Copyright: © Liu 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 6. — Knockdown of MALAT1 promotes cholesterol accumulation by regulating the miR-17-5p/ABCA1 axis in ox-LDL-induced THP-1 macrophages. ABCA1 is a cell membrane protein that mediates the transport of cholesterol, phospholipids and other metabolites from cells to form HDL apolipoproteins. Thus, ABCA1 promotes cholesterol efflux and inhibits macrophage foam cell formation. MALAT1 can sponge miR-17-5p, which targets the 3′-untranslated region of the ABCA1 mRNA, and facilitates its mRNA degradation or translational repression. Knockdown of MALAT1 by small interfering RNA increases ox-LDL uptake, lipid accumulation and total cholesterol levels via the miR-17-5p/ABCA1 axis in ox-LDL-induced macrophages. miR, microRNA; ABCA1, ATP-binding cassette transporter A1; MALAT1, metastasis associated lung adenocarcinoma transcript 1; HDL, high-density lipoprotein; ox-LDL, oxidized low-density lipoprotein.