Isoliquiritigenin Suppresses Oral Squamous Cell Carcinoma Progression by Targeting FABP5-Mediated Lipid Metabolism: Association with the circPOLB/miR-548ae-3p/C-MYC Axis.

Authors

Liang Li, Hong Deng, Zhiyong Li, Yu Li, Lingrui Liu, Lan Xie, Yue Chen

Published in

Oncology research. Volume 34. Issue 8. Pages 27. Epub Jul 16, 2026.

Abstract

Objectives: Oral squamous cell carcinoma (OSCC) is a common and deadly cancer affecting the oral cavity. This study aims to explore the regulatory role and molecular mechanism of miR-548ae-3p in OSCC proliferation, invasion, and lipid metabolism, as well as the therapeutic potential of isoliquiritigenin (ISL) targeting OSCC lipid metabolism. Methods: Expression levels of miR-548ae-3p were measured in OSCC cell lines and normal oral keratinocytes using real-time quantitative polymerase chain reaction. Functional assays, such as cell counting Kit-8 proliferation and Transwell invasion assays, evaluated the effects of miR-548ae-3p overexpression in CAL-27 and SCC-25 cells. Bioinformatic prediction and dual-luciferase reporter assays investigated interactions among miR-548ae-3p, hsa_circRNA_0001794 (circPOLB), and cellular myelocytomatosis oncogene (c-MYC). Lipid metabolism was assessed using lipid droplet staining, fatty acid oxidation assays, total fatty acids and palmitic acid quantification, and fatty acid-binding protein 5 (FABP5) expression analysis. The inhibitory effects of ISL on OSCC lipid metabolism and invasiveness were also examined. Results: MiR-548ae-3p was downregulated in OSCC cells compared to normal keratinocytes (n = 3, p < 0.001). miR-548ae-3p overexpression inhibited the proliferation and invasion of CAL-27 and SCC-25 cells (n = 3, p < 0.001). CircPOLB functions as a molecular sponge for miR-548ae-3p, which in turn targets c-MYC, a key oncogene. MiR-548ae-3p overexpression reduced lipid droplet accumulation, fatty acid oxidation, total fatty acid content, and intracellular palmitic acid levels, accompanied by downregulation of FABP5 (n = 3, p < 0.001). Furthermore, ISL treatment decreased FABP5 expression, fatty acid metabolism, and invasive capacity of OSCC cells (n = 3, p < 0.001), supporting its potential as a therapeutic agent. Conclusions: MiR-548ae-3p displays tumor-suppressive activity in OSCC, restraining proliferation, invasion, and fatty-acid metabolism through engagement of the circPOLB/c-MYC axis and is associated with reduced FABP5 expression. Targeting lipid metabolism using agents like ISL could be a promising approach for treating OSCC.

PMID:
42500563
Bibliographic data and abstract were imported from PubMed on 25 Jul 2026.

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