ArticleThe Journal of experimental medicine2017
CD55 regulates self-renewal and cisplatin resistance in endometrioid tumors.
Article in The Journal of experimental medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 55 papers.
What it found
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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.
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Who cites it
55 citing papers in PubMed, 95 citations in OpenAlex.
- CD55 organizes lipid raft-LCK signaling to potentiate NK-cell antitumor immunity.Cell research · 2026Article
- Stress-induced CD55 supports homologous recombination capacity and drives oxaliplatin resistance in colorectal cancer.Cell communication and signaling : CCS · 2026Article
- Article
- CD55-expressing myeloid-derived suppressor cells (MDSCs) drive cancer immunoevasion.Journal for immunotherapy of cancer · 2026Article
- GDPD5-CD55-EGFR competitive binding axis regulates radioresistance and lipid accumulation in rectal cancer.Cell death & disease · 2026Article
- Complement system in cancer: friend or foe of immunotherapy.Journal for immunotherapy of cancer · 2026Review
- Fueling the Seed: Growth Factors and Cytokines Driving Cancer Stem Cells in Gynecological Malignancies.International journal of molecular sciences · 2025Review
- Patient-derived extracellular matrix from decellularized high-grade serous ovarian carcinoma tissues as a biocompatible support for organoid growth.Translational oncology · 2025Article
- CD55 may be a new target for colorectal cancer treatment.Scientific reports · 2025Article
- The decay-accelerating factor (CD55) in acute leukemia patients and its query implication in cancer pathogenesis.Journal of the Egyptian National Cancer Institute · 2025Article
- Transient inhibition of type I interferon enhances CD8+ T cell stemness and vaccine protection.The Journal of experimental medicine · 2025Article
- Lck Function and Modulation: Immune Cytotoxic Response and Tumor Treatment More Than a Simple Event.Cancers · 2024Review
- Cell surface CD55 traffics to the nucleus leading to cisplatin resistance and stemness by inducing PRC2 and H3K27 trimethylation on chromatin in ovarian cancer.Molecular cancer · 2024Article
- Informed by Cancer Stem Cells of Solid Tumors: Advances in Treatments Targeting Tumor-Promoting Factors and Pathways.International journal of molecular sciences · 2024Review
- Review
- Advances in research on autophagy mechanisms in resistance to endometrial cancer treatment.Frontiers in oncology · 2024Review
- A TOX-ic axis of epigenetic stem cell maintenance and chemoresistance in colon cancer.PLoS biology · 2023Article
- Dual Targeting of Apoptotic and Signaling Pathways in T-Lineage Acute Lymphoblastic Leukemia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Human and murine fibroblast single-cell transcriptomics reveals fibroblast clusters are differentially affected by ageing and serum cholesterol.Cardiovascular research · 2023Article
- LCK facilitates DNA damage repair by stabilizing RAD51 and BRCA1 in the nucleus of chemoresistant ovarian cancer.Journal of ovarian research · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
24 authors at 4 institutions in 1 country.
Funding
Abstract
Effective targeting of cancer stem cells (CSCs) requires neutralization of self-renewal and chemoresistance, but these phenotypes are often regulated by distinct molecular mechanisms. Here we report the ability to target both of these phenotypes via CD55, an intrinsic cell surface complement inhibitor, which was identified in a comparative analysis between CSCs and non-CSCs in endometrioid cancer models. In this context, CD55 functions in a complement-independent manner and required lipid raft localization for CSC maintenance and cisplatin resistance. CD55 regulated self-renewal and core pluripotency genes via ROR2/JNK signaling and in parallel cisplatin resistance via lymphocyte-specific protein tyrosine kinase (LCK) signaling, which induced DNA repair genes. Targeting LCK signaling via saracatinib, an inhibitor currently undergoing clinical evaluation, sensitized chemoresistant cells to cisplatin. Collectively, our findings identify CD55 as a unique signaling node that drives self-renewal and therapeutic resistance through a bifurcating signaling axis and provides an opportunity to target both signaling pathways in endometrioid tumors.
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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.