ArticleCancer informatics2026
Single-Cell Transcriptome Analysis Reveals IRF1-Driven Epithelial States and Glycosaminoglycan-Glycolysis Coupling in Cisplatin-Resistant HGSOC.
Article in Cancer informatics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: Cisplatin resistance is the principal cause of relapse in high-grade serous ovarian cancer (HGSOC), but bulk-expression signatures cannot localize resistant malignant states or the tumor-microenvironment (TME) interactions that sustain them. This study aimed to define cisplatin-resistant epithelial cell states and their regulatory and metabolic circuits by integrating multi-cohort single-cell transcriptomes with pharmacogenomic and clinical data. Methods: We assembled 159,419 cells from 32 HGSOC tumors across six public single-cell RNA-sequencing cohorts and performed harmonized integration, clustering, and lineage annotation. Cisplatin response was mapped to single cells by coupling scRNA-seq data to Genomics of Drug Sensitivity in Cancer predicted cisplatin response score values using Scissor, with AUCell-based validation. We then applied receptor-ligand-based cell-cell communication analysis (CellChat), transcription-factor (TF) activity inference (SCENIC and NetAct with TRRUST), pseudotime trajectory reconstruction (Monocle3), and pathway-level metabolic scoring. Associations with drug sensitivity and patient outcome were evaluated in ovarian cancer cell lines and The Cancer Genome Atlas (TCGA) HGSOC cohort. Results: Among 34 epithelial subclusters, 14 were significantly enriched for a cisplatin-resistant phenotype and collectively accounted for most predicted resistant cells. These states were transcriptionally characterized by stress, interferon, and apoptotic programs and formed dense communication hubs with endothelial cells, fibroblasts, myeloid cells, and T/NK cells via extracellular-matrix and adhesion pathways (for example, LAMA3-CD44, COL6A1/2-CD44, NECTIN3-NECTIN2, and CD99-CD99 interactions). TF-activity modeling converged on an IRF1-centered regulatory program that increased along an epithelial trajectory and coordinated inflammatory and apoptotic gene expression. Metabolically, resistance-enriched epithelial states showed selective up-regulation of glycosaminoglycan biosynthesis, particularly keratan sulfate, coupled to heightened glycolysis; glycolytic activity correlated with predicted cisplatin response score in cell lines and an IRF1/STAT1 readout (GBP3) stratified survival in TCGA HGSOC. Conclusion: Cisplatin resistance in HGSOC is encoded in discrete IRF1-driven epithelial states that are supported by specific TME communication networks and a glycosaminoglycan-glycolysis metabolic axis. This integrative single-cell informatics framework yields testable biomarkers and therapeutic targets for overcoming platinum resistance in ovarian cancer.
Indexed as
Identifiers
What OpenQuestion holds
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.