CircIL4R facilitates the tumorigenesis and inhibits ferroptosis in hepatocellular carcinoma by regulating the miR-541-3p/GPX4 axis.

This study focused on the function of circIL4R dysregulation in tumor progression and ferroptosis of HCC, as well as its molecular mechanism. The quantitative real-time polymerase chain reaction (qRT-PCR) was implemented for measuring RNA expression. Cell proliferation and survival were evaluated using 3-(4, 5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide (MTT). Apoptotic cells were detected via flow cytometry. The quantification of protein expression was executed through western blot. The target binding was assessed via the dual-luciferase reporter, RNA immunoprecipitation (RIP) and RNA pull-down assays. The experiment in vivo was performed using a xenograft model. CircIL4R was abnormally overexpressed in HCC tissues and cells. CircIL4R knockdown impeded oncogenesis and expedited ferroptosis of HCC cells. CircIL4R could directly sponge microRNA-541-3p (miR-541-3p) and miR-541-3p inhibition mitigated the effects of circIL4R knockdown on HCC cells. CircIL4R acted as a miR-541-3p sponge to regulate its target glutathione peroxidase 4 (GPX4). GPX4 up-regulation relieved the miR-541-3p-induced tumor inhibition and ferroptosis aggravation. CircIL4R played an oncogenic role in HCC via the miR-541-3p/GPX4 axis in vivo. Our data suggested that circIL4R served for a tumor promoter and ferroptosis inhibitor in HCC by the miR-541-3p/GPX4 network. This article is protected by copyright. All rights reserved. PMID: 32808701 [PubMed - as supplied by publisher]
Source: Cell Biology International - Category: Cytology Authors: Tags: Cell Biol Int Source Type: research