ArticleCombinatorial chemistry & high throughput screening2025
HRAS Induces Ferroptosis through Upregulating HSPB1 in Hepatocellular Carcinoma.
Article in Combinatorial chemistry & high throughput screening, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed.
- Elevated labile iron contributes to membrane repair deficits in facioscapulohumeral muscular dystrophy.iScience · 2026Article
- Article
- HSPB1 silencing enhances ferroptosis in glioma cells by suppressing BAG3 expression.American journal of translational research · 2025Article
- Targeting cell death mechanisms: the potential of autophagy and ferroptosis in hepatocellular carcinoma therapy.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
backgroundThe aim of this study is to explore the mechanism of HRAS and HSPB1 in ferroptosis. Primary liver cancer is the third leading cause of tumor death worldwide. Hepatocellular carcinoma (HCC) constitutes 75%-85% of cases of primary liver cancer. HRAS and HSPB1 co-express in multiple cells and participate in tumor progression regulation. However, their expression regulation and role in HCC have not been reported.
methodsWe investigated the effects of HRAS and HSPB1 on ferroptosis in in vitro experiments. Here, the role and mechanism of HRAS and HSPB1 on ferroptosis were investigated by transfecting the specific siRNA or overexpressing plasmids in HCC cells.
resultsBioinformatics analysis proved that HRAS and HSPB1 were highly expressed in HCC tissues and associated with poor prognosis of patients with HCC.
conclusionThe regulation of HSPB1 by HRAS enhanced the resistance of HCC cells to ferroptosis. HRAS promoted proliferation and invasion by upregulating HSPB1. This research provides a new potential strategy for HCC treatment.
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Registered trials
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