ArticleFrontiers in medicine2026
LncRNA-PRLB drives ovarian cancer progression and chemoresistance by stabilizing GPX4 mRNA through the FUS-mediated suppression of ferroptosis.
Article in Frontiers in medicine, 2026. 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.
- The Impact of Oxidative Stress Imbalance on Ovarian Function and Its Mechanisms.International journal of general medicine · 2026Review
- Advancing the frontiers of ovarian cancer therapy: a comprehensive synthesis of emerging cell death paradigms.Oncology reviews · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
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Abstract
Background: Ovarian cancer is highly lethal, largely due to the rapid development of paclitaxel resistance. This study aimed to determine whether progression-associated lncRNA in breast cancer (lncRNA-PRLB) regulates ferroptosis and paclitaxel resistance in ovarian cancer and to elucidate the underlying mechanism. Methods: Functional assays, including 5-ethynyl-2'-deoxyuridine (EdU) incorporation, Cell Counting Kit-8 (CCK-8) viability measurements, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, caspase-3 activity assays, Transwell invasion, wound healing, and ferroptosis marker analyses [reactive oxygen species (ROS), malondialdehyde MDA, Fe Results: LncRNA-PRLB was identified as an oncogenic regulator that enhances ovarian cancer cell proliferation, migration, invasion, and paclitaxel resistance. Silencing lncRNA-PRLB induced apoptosis and triggered ferroptosis, characterized by elevated ROS, MDA, Fe Conclusion: This study identifies lncRNA-PRLB as a critical upstream regulator of ferroptosis resistance and chemoresistance in ovarian cancer. By scaffolding FUS to stabilize GPX4 mRNA, lncRNA-PRLB maintains GPX4 expression and enables tumor cells to evade ferroptotic cell death.
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