ArticleCell death discovery2025
SLC25A10 promotes cisplatin resistance by inhibiting ferroptosis in cervical cancer.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Nuclear translocation of SLC25A10 isoform 3 promotes chemoresistance in HCC cells via CEBPB/BCL2A1 signaling.Cell death & disease · 2026Article
- Exploring the Anti-Cervical Cancer Effect and Hepatotoxicity Risk of Gossypol Based on Untargeted Metabolomics and Network Toxicology.Pharmaceuticals (Basel, Switzerland) · 2026Article
- A mitochondrial regulatory network of ferroptosis defense in HPV-positive cervical cancer: therapeutic implications of the mitoSTAT3-DHODH axis.Frontiers in pharmacology · 2026Review
- Mitochondrial reprogramming in cervical cancer: crosstalk with tumor immunity, HPV oncogenic signaling, and therapeutic resistance.Frontiers in immunology · 2026Review
- Inhibin beta A drives colorectal cancer progression through macrophage M2 polarization and mitochondria-dependent ferroptosis suppression.Signal transduction and targeted therapy · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cisplatin (DDP)-based chemotherapy is the standard first-line treatment for cervical cancer (CC). However, many patients with CC develop resistance to DDP, either initially or over time. This resistance significantly limits the effectiveness of treatment. Therefore, identifying new therapeutic targets and combination therapies to overcome DDP resistance is a critical need. In this study, we investigated the expression of SLC25A10 in cervical cancer tissues using bioinformatics analysis and partial tissue analysis. We found that SLC25A10 expression was significantly higher in human cervical cancer tissues compared to normal tissues, based on data from The Cancer Genome Atlas (TCGA) and clinical samples. Moreover, increased SLC25A10 expression was associated with adverse clinicopathological characteristics of cervical cancer patients. To explore the functional role of SLC25A10, we conducted a series of in vitro and in vivo experiments. Our results demonstrated that SLC25A10 promotes cervical cancer cell growth, migration, and resistance to DDP. Mechanistically, we found that inhibiting SLC25A10 expression restricted the transport of glutathione (GSH) and reduced the expression of glutathione peroxidase 4 (GPX4). This led to increased intracellular lipid peroxidation and accumulation of reactive oxygen species (ROS), ultimately promoting iron-mediated cell death (ferroptosis) in cervical cancer cells. In conclusion, our findings suggest that SLC25A10 may serve as a novel therapeutic target to overcome cisplatin resistance and enhance the efficacy of chemotherapy in CC. Future studies should focus on further elucidating the role of SLC25A10 in CC and exploring its potential as a therapeutic target in combination with other treatments.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.