HNRNPL facilitates ferroptosis in hepatocellular carcinoma cells by promoting S100A9 expression
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View abstract on PubMed
Summary
This summary is machine-generated.Heterogeneous nuclear ribonucleoprotein L (HNRNPL) promotes ferroptosis in hepatocellular carcinoma (HCC) by stabilizing S100A9 mRNA. This finding reveals a novel mechanism driving HCC progression and offers potential therapeutic targets.
Area Of Science
- Molecular oncology
- Cell death pathways
- Cancer biology
Background
- Hepatocellular carcinoma (HCC) is a major global health concern with limited effective treatments.
- Ferroptosis, a regulated form of cell death, is implicated in cancer progression and therapy resistance.
- The role of specific RNA-binding proteins in regulating ferroptosis in HCC remains incompletely understood.
Purpose Of The Study
- To investigate the impact of heterogeneous nuclear ribonucleoprotein L (HNRNPL) on ferroptosis in HCC cells.
- To elucidate the underlying molecular mechanisms by which HNRNPL influences ferroptosis.
- To evaluate the therapeutic potential of targeting HNRNPL in HCC.
Main Methods
- Analysis of HNRNPL and S100A9 expression in HCC tissues and cells.
- In vitro assays measuring cell activity, reactive oxygen species (ROS), iron content, lipid peroxidation (LPO), malondialdehyde (MDA), and glutathione (GSH) levels.
- RNA immunoprecipitation (RIP), RNA pull-down, and actinomycin D assays to determine HNRNPL-S100A9 interaction and mRNA stability.
- In vivo xenograft tumor experiments in nude mice.
Main Results
- HNRNPL and S100A9 were significantly overexpressed in HCC.
- HNRNPL knockdown decreased HCC cell activity and promoted ferroptosis markers (increased iron, LPO, MDA, ROS; decreased GSH, GPX4, SLC7A11).
- HNRNPL enhanced S100A9 mRNA stability and expression; S100A9 overexpression or ferroptosis inhibition reversed HNRNPL knockdown effects.
- In vivo, reduced HNRNPL expression inhibited tumor growth.
Conclusions
- HNRNPL promotes ferroptosis in HCC cells by increasing S100A9 mRNA stability and expression via RNA-binding protein (RBP) action.
- Targeting HNRNPL represents a potential therapeutic strategy for hepatocellular carcinoma.
- This study uncovers a novel regulatory axis in HCC ferroptosis.
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