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Dysregulation of RNA Editing Contributes to Platinum Resistance in Ovarian Cancer [scRNA-seq]

ABSTRACT: This study investigates the role of RNA editing in platinum-resistant ovarian cancer.

ORGANISM(S): Mus musculus

PROVIDER: GSE311360 | GEO | 2026/05/23

REPOSITORIES: GEO

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Dysregulation of RNA Editing Contributes to Platinum Resistance in Ovarian Cancer

Project description:This study investigates the role of RNA editing in platinum-resistant ovarian cancer.

2026-05-23 | GSE308999 | GEO

Dysregulation of RNA Editing Contributes to Platinum Resistance in Ovarian Cancer

Project description:Dysregulation of RNA Editing Contributes to Platinum Resistance in Ovarian Cancer

| PRJNA1333685 | ENA

Dysregulation of RNA Editing Contributes to Platinum Resistance in Ovarian Cancer [scRNA-seq]

Project description:Dysregulation of RNA Editing Contributes to Platinum Resistance in Ovarian Cancer [scRNA-seq]

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USP18 impacts on platinum-resistance in ovarian cancer cells by modulating DNA repair

Project description:Aims: Deubiquitinases (DUBs) are proteases with emerging roles in cancer progression and therapy resistance, yet their contribution to drug resistance in ovarian cancer remains underexplored. Ovarian cancer patients often fail to benefit from platinum-based therapy, highlighting the need to identify novel factors involved in drug resistance. To this end we performed a CRISPR/Cas9 screen targeting DUB family to identify genes essential for platinum- resistant ovarian carcinoma cell survival. Methods: A CRISPR/CAS9 DUB knockout screen was performed on IGROV-1 parental and platinum-resistant ovarian carcinoma cells. Preclinical pharmacology approaches were also applied. Results: We identified USP18 as a survival factor in platinum-resistant ovarian cancer cells. USP18 expression was elevated at the mRNA and protein levels across five platinum-resistant cell lines. Knockdown and CRISPR/CAS9 editing of USP18 sensitized cells to cisplatin, coinciding with impaired repair of cisplatin-induced DNA damage. RNA-seq of USP18 RNA interfered and edited cells revealed the modulation of pathways including DNA repair. A peptide-based USP18 inhibitor suppressed growth of resistant cells, supporting its role in sustaining the growth of platinum-resistant cells. Conclusion: We identified USP18 as a novel mediator of platinum resistance in ovarian cancer, through modulating DNA repair. Targeting USP18 may offer a therapeutic strategy to improve outcomes in platinum-resistant ovarian cancer.

2026-05-29 | GSE326132 | GEO

Gene expression profiles of platinum-resistant high-grade serous ovarian carcinoma

Project description:Ovarian cancer is one of the leading causes of death in females in the world. High-grade serous ovarian carcinoma (HGSOC) is the most common histological subtype, and platinum platinum-resistance is a clinical challenge, In this study, we investigated the gene expression profiles of platinum-resistant and platinum-sensitive HGSOC.

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MicroRNA sequencing for platinum-resistant high-grade serous ovarian carcinoma

Project description:Ovarian cancer is one of the leading causes of death in females in the world. High-grade serous ovarian carcinoma (HGSOC) is the most common histological subtype, and the platinum-resistance is a clinical challenge, In this study, we investigated the microRNA (miRNA) profiles of platinum-resistant and platinum-sensitive HGSOC.

2025-09-03 | GSE273635 | GEO

DNA Methylatransferase Inhibition Prevents Platinum-Induced Ovarian Cancer Stem Cell Enrichment

Project description:Platinum-based therapy is the standard first-line treatment for high-grade serous ovarian cancer (HGSC). However, most patients develop resistance and recurrence despite an initial response to therapy. Ovarian cancer stem cells (OCSCs) are enriched in recurrent tumors and contribute to platinum resistance. These tumors also show promoter DNA hypermethylation, and DNA methyltransferase inhibitors (DNMTis) have been shown to restore sensitivity in platinum-resistant ovarian cancer cells. Here, we demonstrated that combining DNMTi with platinum prevented the platinum-induced enrichment of OCSCs and identified NF-κB and STAT3 signaling pathways as potential regulators of platinum-induced OCSC enrichment. STAT3 was active at baseline in OC cells and platinum treatment alone activated NF-κB while maintaining STAT3 activity. Platinum combined with DNMTi decreased STAT3 activation, while still inducing NF-κB activation. Knockdown experiments demonstrated that the presence of both NF-κB and STAT3 was necessary for platinum-induced OCSC enrichment. Analysis of STAT3 and NF-κB subunit p65 CUT&RUN data showed increased binding in introns and intergenic regions in response to platinum. Additionally, DNMTi enriched NF-κB binding at endogenous retroviruses (ERVs), which correlated with changes in expression of nearby genes when DNMTi was combined with platinum. We conclude that combining DNMTi with platinum modulates STAT3 and NF-κB activation and genomic binding, potentially influencing target gene expression and preventing platinum-induced enrichment of OCSCs.

2026-06-22 | GSE332978 | GEO

microRNA profiling of platinum sensitive and platinum resistant high grade serous ovarian cancer samples

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2020-02-11 | E-MTAB-7084 | biostudies-arrayexpress

Transcriptional profiling of platinum sensitive and platinum resistant high grade serous ovarian cancer samples

Project description:This study aims at correlating changes in the transcriptional state in high grade serous epithelial ovarian cancer (HGS-EOC) to the response to therapy, in particular the insurgence of resistance to platinum-based treatment.

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RNA-Seq of treatment response of platinum sensitive and platinum resistant ovarian cancer cells

Project description:Resistance to platinum-based chemotherapy is a clinical challenge in the treatment of ovarian cancer (OC) and limits survival. Therefore, innovative drugs against platinum-resistance are urgently needed. Our therapeutic concept is based on the conjugation of two chemotherapeutic compounds to a monotherapeutic pro-drug, which is taken up by cancer cells and cleaved into active cytostatic metabolites. Here, we explore the activity of the duplex-prodrug 5-FdU-ECyd, covalently linking 2'-deoxy-5-fluorouridine (5-FdU) and 3'-C-ethynylcytidine (ECyd), on platinum-resistant OC cells. RNA-Sequencing was used for characterization of 5-FdU-ECyd treated platinum-sensitive A2780 and isogenic platinum-resistant A2780cis.

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