ArticleMolecular cancer2024
Cell surface CD55 traffics to the nucleus leading to cisplatin resistance and stemness by inducing PRC2 and H3K27 trimethylation on chromatin in ovarian cancer.
Article in Molecular cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- CD55 organizes lipid raft-LCK signaling to potentiate NK-cell antitumor immunity.Cell research · 2026Article
- Cuproptosis-mediated stemness inhibition by a self-assembled herbal nanoplatform overcomes chemoresistance in ovarian cancer.Materials today. Bio · 2026Article
- Development of a noninvasive murine model of hyperthermic intraperitoneal chemotherapy (HIPEC) treatment for ovarian cancer.Research square · 2026Article
- EGFR-dependent delivery of phosphorylated IGFBP3 by cancer stem cells drives chemotherapy resistance in colorectal cancer.Cell death & disease · 2026Article
- The Complosome: An Emerging Intracellular Complement Network in Cancer Development and Therapy.International journal of molecular sciences · 2026Review
- CD55-expressing myeloid-derived suppressor cells (MDSCs) drive cancer immunoevasion.Journal for immunotherapy of cancer · 2026Article
- Th17-related genes PGAP1 and TMBIM1 serve as potential diagnostic and predictive biomarkers in systemic sclerosis: bioinformatic identification and murine model validation.Clinical rheumatology · 2026Article
- Platinum-resistant ovarian cancer: From mechanisms to treatment strategies.Genes & diseases · 2026Review
- Identification of serum peptide biomarkers for cholangiocarcinoma diagnosis and staging via MALDI-TOF MS and LC-MS/MS.British journal of cancer · 2026Article
- Advancing Intervertebral Disc Biology via Omics: Implications for Nucleus Pulposus Progenitor Cell-Based Regeneration.JOR spine · 2025Review
- Cancer-associated fibroblasts are associated with neo-adjuvant treatment response in oesophageal adenocarcinoma.British journal of cancer · 2025Article
- Cell Surface Proteomics Reveals Hypoxia-Regulated Pathways in Cervical and Bladder Cancer.Proteomes · 2025Article
- CD55 may be a new target for colorectal cancer treatment.Scientific reports · 2025Article
- Epigenetics-targeted drugs: current paradigms and future challenges.Signal transduction and targeted therapy · 2024Review
- Divergent Processing of Cell Stress Signals as the Basis of Cancer Progression: Licensing NFκB on Chromatin.International journal of molecular sciences · 2024Review
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22 authors.
Funding
Abstract
backgroundPlatinum resistance is the primary cause of poor survival in ovarian cancer (OC) patients. Targeted therapies and biomarkers of chemoresistance are critical for the treatment of OC patients. Our previous studies identified cell surface CD55, a member of the complement regulatory proteins, drives chemoresistance and maintenance of cancer stem cells (CSCs). CSCs are implicated in tumor recurrence and metastasis in multiple cancers.
methodsProtein localization assays including immunofluorescence and subcellular fractionation were used to identify CD55 at the cell surface and nucleus of cancer cells. Protein half-life determinations were used to compare cell surface and nuclear CD55 stability. CD55 deletion mutants were generated and introduced into cancer cells to identify the nuclear trafficking code, cisplatin sensitivity, and stem cell frequency that were assayed using in vitro and in vivo models. Detection of CD55 binding proteins was analyzed by immunoprecipitation followed by mass spectrometry. Target pathways activated by CD55 were identified by RNA sequencing.
resultsCD55 localizes to the nucleus of a subset of OC specimens, ascites from chemoresistant patients, and enriched in chemoresistant OC cells. We determined that nuclear CD55 is glycosylated and derived from the cell surface pool of CD55. Nuclear localization is driven by a trafficking code containing the serine/threonine (S/T) domain of CD55. Nuclear CD55 is necessary for cisplatin resistance, stemness, and cell proliferation in OC cells. CD55 S/T domain is necessary for nuclear entry and inducing chemoresistance to cisplatin in both in vitro and in vivo models. Deletion of the CD55 S/T domain is sufficient to sensitize chemoresistant OC cells to cisplatin. In the nucleus, CD55 binds and attenuates the epigenetic regulator and tumor suppressor ZMYND8 with a parallel increase in H3K27 trimethylation and members of the Polycomb Repressive Complex 2.
conclusionsFor the first time, we show CD55 localizes to the nucleus in OC and promotes CSC and chemoresistance. Our studies identify a therapeutic mechanism for treating platinum resistant ovarian cancer by blocking CD55 nuclear entry.
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