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LncRNA LEF1‐AS1 regulates the migration and proliferation of vascular smooth muscle cells by targeting miR‐544a/PTEN axis
Author(s) -
Zhang Lina,
Zhou Changyong,
Qin Qiaoji,
Liu Zhenfang,
Li Peng
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28728
Subject(s) - pten , cell growth , microrna , cancer research , protein kinase b , western blot , downregulation and upregulation , vascular smooth muscle , cell , cell migration , biology , microbiology and biotechnology , chemistry , signal transduction , pi3k/akt/mtor pathway , smooth muscle , gene , endocrinology , genetics
Long noncoding RNAs (lncRNAs) play important roles in endothelium development. A lncRNA, LEF1‐AS1, is recently emerging as a potent mediator of the proliferation and migration of a number of cells, including smooth muscle cells. However, the effects of LEF1‐AS1 in atherosclerosis remains largely unknown. Specimens from patients with coronary artery atherosclerosis were collected. The quantitative real‐time polymerase chain reaction was used to analyze levels of LEF1‐AS1 and microRNA‐544a (miR‐544a). Western blot analysis was used to assess PTEN, P‐Akt, and T‐Akt protein expression. Proliferation, migration, and invasion of cells were analyzed by cell counting kit‐8 assay, scratch wound assay, and transwell assay, respectively. The interaction between LEF1‐AS1, miR‐544a, and PTEN was probed using bioinformatical analysis and dual‐luciferase assay. In plasma and tissue of patients with coronary artery atherosclerosis, LEF1‐AS1 was upregulated and miR‐544a was downregulated. A negative correlation was found between LEF1‐AS1 and miR‐544a. miR‐544a overexpression reversed the inhibition of LEF1‐AS1 in smooth muscle cell proliferation and invasion, which were mediated through the PTEN pathway. LEF1‐AS1 regulates smooth muscle cell proliferation and migration through the miR‐544a/PTEN axis, indicating that LEF1‐AS1 may be a potential therapeutic target in atherosclerosis.