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PGM5 - AS1 regulates ferroptosis - Mediated gastric cancer cell behavior via ERK signaling pathway
Shichen Sun1, Mengying Luo2, Xiuzhu Zhan3
1Department of Breast Radiotherapy, Liaoning Cancer Hospital and Institution, Shenyang 110000, China.
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 (Fe2+), 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.
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