LINC02266 promotes proliferation and metastasis and inhibits ferroptosis of gastric cancer cells by regulating AKT/ACSL4 pathway
- PMID: 40682711
- DOI: 10.1007/s11010-025-05354-4
LINC02266 promotes proliferation and metastasis and inhibits ferroptosis of gastric cancer cells by regulating AKT/ACSL4 pathway
Abstract
Ferroptosis is a novel form of cell death characterized by iron-dependent oxidative damage, lipid peroxidation, and the accumulation of reactive oxygen species. There exists a close correlation between ferroptosis and gastric cancer (GC). Recent research has shown that many ferroptosis-related long non-coding RNAs (lncRNAs) affect the occurrence and progression of GC. However, the exact mechanism has not been elucidated. This study showed that a novel lncRNA LINC02266 was upregulated in GC cells and was a key lncRNA associated with GC prognosis and progression. Functional analysis indicated that LINC02266 suppressed ferroptosis and promoted GC cell proliferation, migration, invasion, and tumor growth in vitro and vivo. Mechanistically, we found that LINC02266 inhibited erastin-induced ferroptosis by suppressing ACSL4 levels, which may be related to the AKT pathway. This study indicates that LINC02266 can serve as a diagnostic marker and novel therapeutic target for GC.
Keywords: ACSL4; Ferroptosis; Gastric cancer; Invasion and migration; LINC02266.
© 2025. The Author(s).
Conflict of interest statement
Declarations. Conflict of interest: All authors declare they have no competing interests. Ethical approval: All animal experiments were approved by the Animal Experimental Research Ethics Committee of Shandong Second Medical University and conducted according to its guidelines (Approval No.2024SDL009). This study conforms to the Helsinki Declaration of the World Medical Association.
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