ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
HSPB1/KDM1 A facilitates ANXA2 expression via hypomethylated DNA promoter to inhibit ferroptosis and enhance gemcitabine resistance in pancreatic cancer.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Integrated single-cell analysis with experimental validation reveals ANXA2 as a therapeutic target for ferroptosis in inflammatory bowel disease.American journal of translational research · 2026Article
- Article
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Authors and funding
3 authors.
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Abstract
Chemotherapy resistance contributes to the unsatisfied prognosis in pancreatic cancer (PC) patients. Heat shock protein beta-1 (HSPB1) plays a tumor promoting role in PC by inhibiting ferroptosis. This study aims to explore whether high expression of HSPB1 was responsible for ferroptosis and gemcitabine (GEM) resistance in PC. Here, we found that HSPB1 was upregulated in GEM-resistant PC cells and tumor tissues, as confirmed by RT-qPCR and Western blotting assays. Knockdown of HSPB1 enhanced GEM sensitivity, decreased the abilities of proliferation and invasion, and promoted apoptosis in GEM-resistant PC cells. Utilizing commercial kits, HSPB1 inhibition triggered ferroptosis, as indicated by increased levels of reactive oxygen species, malondialdehyde, and Fe
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