LUCAT1 contributes to MYRF-dependent smooth muscle cell apoptosis and may facilitate aneurysm formation via the sequestration of miR-199a-5p.

Abstract

The overwhelming number of interrogations reveals the implication of long noncoding RNAs (lncRNAs) in diverse malignancies, little is unveiled about lncRNAs participation in the abdominal aortic aneurysm (AAA). The study aimed to monitor the role and responsible mechanism of LUCAT1 in AAA. The cellular function of LUCAT1 on smooth muscle cells (SMCs) proliferation and apoptosis were examined through the conduction of CCK-8, EdU, TUNEL, and caspase-3 activity assays. LUCAT1 depletion was observed to boost SMCs proliferation or suppress SMCs apoptosis. The opposite results on SMCs proliferation and apoptosis were achieved in response to LUCAT1 promotion. The abundance of LUCAT1 in the cytoplasm was ascertained by subcellular fractionation and FISH analyses on the basis of LncLocator prediction. The binding of LUCAT1 to miR-199a-5p predicted by DIANA and starbase was certified by luciferase reporter assay and RIP analysis. Besides, multiple prediction tools unveiled the interaction between miR-199a-5p and myelin regulatory factor (MYRF). Quantitative real-time polymerase chain reaction uncovered the suppressive effect of miR-199a-5p and the positive regulation of LUCAT1 on MYRF expression. Rescue experiments revealed that LUCAT1 depletion pose suppression on SMCs apoptosis and MYRF elevation abrogated this suppression induced by LUCAT1 inhibition. These findings unmasked that the pro-apoptosis impact of LUCAT1 in SMCs via directly targeting miR-199a-5p to elevate MYRF expression, which may provide valuable information on AAA prevention.