ArticlePloS one2021
Epigenetic suppression of SLFN11 in germinal center B-cells during B-cell development.
Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 32 citations in OpenAlex.
- Article
- Integrative analysis of SLFN11-related DEGs reveals novel biomarkers for cisplatin sensitivity and immune modulation in colorectal cancer.Cancer cell international · 2026Article
- Schlafen 11 as a prognostic and potentially predictive biomarker in soft tissue sarcoma: evidence from a real-world cohort.Frontiers in oncology · 2026Article
- Co-expression of CD30 and SLFN11 serves as a dual biomarker for the treatment of cutaneous T-cell lymphoma.NAR cancer · 2025Article
- Epigenetic and Post-Translational Regulation of Schlafen Family Expression and Their Differential Methods of Regulating Proteins.International journal of molecular sciences · 2025Review
- SLFN11, far from being limited to responding to cancer DNA damage.Clinical and experimental medicine · 2025Review
- SLFN11-mediated ribosome biogenesis impairment induces TP53-independent apoptosis.Molecular cell · 2025Article
- NEAT1 and CHROMR lncRNAs: a promising diagnostic tool for diffuse large B-cell lymphoma especially in elderly patients.Biomarkers in medicine · 2024Article
- Article
- KLC1-ROS1 Fusion Exerts Oncogenic Properties of Glioma Cells via Specific Activation of JAK-STAT Pathway.Cancers · 2023Article
- The crucial role of single-stranded DNA binding in enhancing sensitivity to DNA-damaging agents for Schlafen 11 and Schlafen 13.iScience · 2023Article
- Schlafen 11 (SLFN11) Kills Cancer Cells Undergoing Unscheduled Re-replication.Molecular cancer therapeutics · 2023Article
- Epigenetic upregulation of Schlafen11 renders WNT- and SHH-activated medulloblastomas sensitive to cisplatin.Neuro-oncology · 2023Article
- Successful Treatment of Acute Uric Acid Nephropathy with Rasburicase in a Primary Central Nervous System Lymphoma Patient Showing a Dramatic Response to Methotrexate-Case Report.Journal of clinical medicine · 2022Article
- Reconsidering the mechanisms of action of PARP inhibitors based on clinical outcomes.Cancer science · 2022Review
- Can Schlafen 11 Help to Stratify Ovarian Cancer Patients Treated with DNA-Damaging Agents?Cancers · 2022Review
- Schlafens Can Put Viruses to Sleep.Viruses · 2022Review
- Prognostic impact of Schlafen 11 in bladder cancer patients treated with platinum-based chemotherapy.Cancer science · 2022Article
- SLFN11's surveillance role in protein homeostasis.Oncoscience · 2022Article
- A wake-up call for cancer DNA damage: the role of Schlafen 11 (SLFN11) across multiple cancers.British journal of cancer · 2021Review
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundSLFN11 has recently been reported to execute cancer cells harboring replicative stress induced by DNA damaging agents. However, the roles of SLFN11 under physiological conditions remain poorly understood. Germinal center B-cells (GCBs) undergo somatic hypermutations and class-switch recombination, which can cause physiological genotoxic stress. Hence, we tested whether SLFN11 expression needs to be suppressed in GCBs during B-cell development.
objectiveTo clarify the expression profile of SLFN11 in different developmental stages of B-cells and B-cell-derived cancers.
methodsWe analyzed the expression of SLFN11 by mining cell line databases for different stages of normal B-cells and various types of B-cell-derived cancer cell lines. We performed dual immunohistochemical staining for SLFN11 and B-cell specific markers in normal human lymphatic tissues. We tested the effects of two epigenetic modifiers, an EZH2 inhibitor, tazemetostat (EPZ6438) and a histone deacetylase inhibitor, panobinostat (LBH589) on SLFN11 expression in GCB-derived lymphoma cell lines. We also examined the therapeutic efficacy of these drugs in combination with cytosine arabinoside and the effects of SLFN11 on the efficacy of cytosine arabinoside in SLFN11-overexpressing cells.
resultsSLFN11 mRNA level was found low in both normal GCBs and GCB-DLBCL (GCB like-diffuse large B-cell lymphoma). Immunohistochemical staining showed low SLFN11 expression in GCBs and high SLFN11 expression in plasmablasts and plasmacytes. The EZH2 and HDAC epigenetic modifiers upregulated SLFN11 expression in GCB-derived lymphoma cells and made them more susceptible to cytosine arabinoside. SLFN11 overexpression further sensitized GCB-derived lymphoma cells to cytosine arabinoside.
conclusionsThe expression of SLFN11 is epigenetically suppressed in normal GCBs and GCB-derived lymphomas. GCB-derived lymphomas with low SLFN11 expression can be treated by the combination of epigenetic modifiers and cytosine arabinoside.
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