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PGM5 - AS1 regulates ferroptosis - Mediated gastric cancer cell behavior via ERK signaling pathway.

Cellular signalling 2026 Vol.138() p. 112167

Sun S, Luo M, Zhan X, Wang Q, Yang X

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[BACKGROUND] Gastric cancer (GC) remains a globally significant malignancy with high morbidity.

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APA Sun S, Luo M, et al. (2026). PGM5 - AS1 regulates ferroptosis - Mediated gastric cancer cell behavior via ERK signaling pathway.. Cellular signalling, 138, 112167. https://doi.org/10.1016/j.cellsig.2025.112167
MLA Sun S, et al.. "PGM5 - AS1 regulates ferroptosis - Mediated gastric cancer cell behavior via ERK signaling pathway.." Cellular signalling, vol. 138, 2026, pp. 112167.
PMID 41086958

Abstract

[BACKGROUND] Gastric cancer (GC) remains a globally significant malignancy with high morbidity. Long non-coding RNAs (lncRNAs) are increasingly recognized as pivotal modulators in tumor biology. However, the involvement of phosphoglucomutase 5 antisense RNA 1 (PGM5-AS1) in regulating ferroptosis in GC has not been comprehensively clarified.

[METHODS] The Cancer Genome Atlas database was analyzed to identify PGM5-AS1. Polymerase chain reaction, fluorescence in situ hybridization, and multiple cell-based assays were performed. Western blotting, lipid peroxidation staining, reactive oxygen species, ferrous ion (Fe, and malondialdehyde detection were employed. Animal experiments were also conducted.

[RESULTS] Reduced levels of PGM5-AS1 were linked to ferroptosis in GC cells. Overexpression of PGM5-AS1 markedly suppressed cell growth and invasiveness, whereas its silencing led to enhanced tumorigenic traits. PGM5-AS1 mediated ferroptosis through the extracellular signal-regulated kinase signaling pathway.

[CONCLUSION] PGM5 - AS1 and its regulatory axis are critical in GC progression and may serve as a promising target for therapeutic intervention.

MeSH Terms

Stomach Neoplasms; Ferroptosis; Humans; Cell Line, Tumor; MAP Kinase Signaling System; Animals; Mice, Nude; RNA, Long Noncoding; Mice; Cell Proliferation; Gene Expression Regulation, Neoplastic; Reactive Oxygen Species; Mice, Inbred BALB C

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