---
title: "SLFN11 as a biomarker of cisplatin sensitivity in pediatric solid tumors"
id: "british-journal-of-cancer-0-slfn11-enhances-cisplatin-sensitivity-in-pediatric-cancer-via-activation-of"
canonical_url: "https://medichelpline.com/clinical-feed/british-journal-of-cancer-0-slfn11-enhances-cisplatin-sensitivity-in-pediatric-cancer-via-activation-of"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "British Journal of Cancer"
source_url: "https://www.nature.com/articles/s41416-026-03571-2"
published_at: "2026-09-02T12:00:00.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# SLFN11 as a biomarker of cisplatin sensitivity in pediatric solid tumors
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/british-journal-of-cancer-0-slfn11-enhances-cisplatin-sensitivity-in-pediatric-cancer-via-activation-of
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** British Journal of Cancer
- **Source URL:** [Original Journal Publication](https://www.nature.com/articles/s41416-026-03571-2)
- **Published At:** 2026-09-02T12:00:00.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- The study examines **SLFN11**, a DNA/RNA helicase-like protein, in paediatric solid tumours (Wilms tumour, osteosarcoma, medulloblastoma) to evaluate its role as a predictive biomarker for DNA-damaging agents such as **cisplatin** and the **PARP inhibitor talazoparib**. - Public datasets (TARGET, ICGC) were analysed for SLFN11 expression correlations with patient survival; results were tumour type–specific, with SLFN11 acting as a positive, negative, or neutral predictor depending on context. - In paediatric cancer cell lines, baseline **SLFN11** expression and promoter methylation were measured; promoter methylation was identified as a regulator of SLFN11 expression similar to observations in adult cancers. - Functional restoration of SLFN11 using CRISPR-dCas9-mediated activation sensitised tested cell lines from three tumour types to **cisplatin** and **talazoparib**, indicating SLFN11 can dictate chemosensitivity. - Transcriptomic profiling under cisplatin exposure showed SLFN11 modulates the DNA damage response and **MAPK signalling**, enhancing chemotherapy cytotoxicity via activation of stress-response pathways and suppression of survival pathways. - SLFN11 is regulated epigenetically (promoter methylation, PRC-mediated histone methylation, histone deacetylation) and transcriptionally (including induction by interferon-γ), linking DNA damage response and innate immunity. - Prior literature cited: SLFN11 blocks stressed replication forks, interacts with replication proteins, and opens chromatin to activate immediate early genes leading to cell cycle arrest; its silencing confers resistance to DDAs and PARP inhibitors. - The study concludes SLFN11 is a context-dependent predictive biomarker and a potential therapeutic target to overcome chemoresistance in paediatric solid tumours; specific numerical results, detailed methods, and full data were not reported in the provided source excerpt.
## Clinical Analysis & Structured Key Points
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[nature](https://www.nature.com/) 2. [british journal of cancer](https://www.nature.com/bjc) 3. [articles](https://www.nature.com/bjc/articles?type=article) 4. article SLFN11 enhances cisplatin sensitivity in pediatric cancer via activation of stress-response and suppression of survival pathways [ Download PDF ](https://www.nature.com/articles/s41416-026-03571-2.pdf) [ Download PDF ](https://www.nature.com/articles/s41416-026-03571-2.pdf) * Article * [Open access](https://www.springernature.com/gp/open-science/about/the-fundamentals-of-open-access-and-open-research) * Published: 02 September 2026 Molecular Diagnostics # SLFN11 enhances cisplatin sensitivity in pediatric cancer via activation of stress-response and suppression of survival pathways * [Ayesha Jabeen](https://www.nature.com/articles/s41416-026-03571-2#auth-Ayesha-Jabeen-Aff1)[1](https://www.nature.com/articles/s41416-026-03571-2#Aff1) [na1](https://www.nature.com/articles/s41416-026-03571-2#na1), * [Dina Awartani](https://www.nature.com/articles/s41416-026-03571-2#auth-Dina-Awartani-Aff1-Aff2)[1](https://www.nature.com/articles/s41416-026-03571-2#Aff1),[2](https://www.nature.com/articles/s41416-026-03571-2#Aff2) [na1](https://www.nature.com/articles/s41416-026-03571-2#na1), * [Shimaa Sherif](https://www.nature.com/articles/s41416-026-03571-2#auth-Shimaa-Sherif-Aff1)[1](https://www.nature.com/articles/s41416-026-03571-2#Aff1), * [Eiman I. Ahmed](https://www.nature.com/articles/s41416-026-03571-2#auth-Eiman_I_-Ahmed-Aff1-Aff3)[1](https://www.nature.com/articles/s41416-026-03571-2#Aff1),[3](https://www.nature.com/articles/s41416-026-03571-2#Aff3), * [Rania Alanany](https://www.nature.com/articles/s41416-026-03571-2#auth-Rania-Alanany-Aff1-Aff2)[1](https://www.nature.com/articles/s41416-026-03571-2#Aff1),[2](https://www.nature.com/articles/s41416-026-03571-2#Aff2), * [Ayman Saleh](https://www.nature.com/articles/s41416-026-03571-2#auth-Ayman-Saleh-Aff4)[4](https://www.nature.com/articles/s41416-026-03571-2#Aff4), * [Wouter R. L. Hendrickx](https://www.nature.com/articles/s41416-026-03571-2#auth-Wouter_R__L_-Hendrickx-Aff1-Aff2) [ORCID: orcid.org/0000-0002-7649-5092](https://orcid.org/0000-0002-7649-5092)[1](https://www.nature.com/articles/s41416-026-03571-2#Aff1),[2](https://www.nature.com/articles/s41416-026-03571-2#Aff2) & * … * [Christophe M. Raynaud](https://www.nature.com/articles/s41416-026-03571-2#auth-Christophe_M_-Raynaud-Aff1) [ORCID: orcid.org/0000-0003-1551-8075](https://orcid.org/0000-0003-1551-8075)[1](https://www.nature.com/articles/s41416-026-03571-2#Aff1) Show authors [_British Journal of Cancer_](https://www.nature.com/bjc) (2026) [Cite this article](https://www.nature.com/articles/s41416-026-03571-2#citeas) [ Save article ](https://www.nature.com/articles/s41416-026-03571-2/save-research?_csrf=FabQNnZ4CFr_EXvhEDdHvXkBvXxRDFvc) [ View saved research ](https://www.nature.com/saved-research) ## Abstract ### Background Paediatric cancers pose treatment challenges due to biological heterogeneity and variable chemotherapy responses. SLFN11, a DNA/RNA helicase-like protein known to sensitise adult tumours to DNA-damaging agents, remains underexplored in paediatric malignancies. ### Methods We examined SLFN11 in Wilms tumour, osteosarcoma, and medulloblastoma using bioinformatics, epigenetic profiling and functional assays. Public datasets (TARGET, ICGC) were analysed to assess SLFN11 expression in relation to survival. Paediatric cancer cell lines were evaluated for baseline expression and promoter methylation. CRISPR-dCas9-mediated activation was used to restore SLFN11, and chemosensitivity was tested with cisplatin and the PARP inhibitor talazoparib. Transcriptomic profiling under cisplatin exposure was performed to identify pathways regulated by SLFN11. ### Results SLFN11 showed tumour type–specific correlations with patient outcome, acting as a positive, negative, or neutral predictor depending on cancer context. Promoter methylation regulated SLFN11 expression in paediatric cancers similarly to adult tumours. SLFN11 activation sensitised all three functionally tested cell lines to cisplatin and talazoparib, with transcriptomics showing its role in DNA damage response and MAPK signalling to enhance chemotherapy cytotoxicity. ### Conclusion In paediatric solid tumours, SLFN11 is a potential predictive biomarker of treatment response. Its ability to dictate the _DNA damage landscape_ through epigenetic modulation highlights its significance as a target for overcoming _chemoresistance_ and improving therapeutic efficacy in young patients. SLFN11 functions as a context-dependent biomarker of outcome and chemotherapy response in paediatric solid tumours. Its epigenetic regulation and modulation of DNA damage highlights SLFN11 as a therapeutic target to overcome chemoresistance. ### Explore related subjects Discover the latest articles and news in related subjects. * [Oncology](https://www.nature.com/subjects/oncology) * [Paediatric cancer](https://www.nature.com/subjects/paediatric-cancer) ## Introduction SLFN11, initially identified as a putative DNA/RNA helicase localised in the nucleus, gained prominence in 2012 when its expression was linked to sensitivity to DNA-damaging agents (DDAs), including platinum-based drugs like cisplatin and PARP inhibitors such as talazoparib [[1](https://www.nature.com/articles/s41416-026-03571-2#ref-CR1 "Zoppoli G, Regairaz M, Leo E, Reinhold WC, Varma S, Ballestrero A, et al. Putative DNA/RNA helicase Schlafen-11 \(SLFN11\) sensitizes cancer cells to DNA-damaging agents. Proc Natl Acad Sci USA. 2012;109:15030–5. https://doi.org/10.1073/pnas.1205943109 .")]. Since this seminal work SLFN11 was extensively studied. During replication stress, SLFN11 binds to Replication Protein A at stalled replication forks and interacts with MCM3 and DHX9. These interactions facilitate chromatin remodelling around replication initiation sites, activating the transcription of immediate early genes and inducing cell cycle arrest [[2](https://www.nature.com/articles/s41416-026-03571-2#ref-CR2 "Murai J, Tang S-W, Leo E, Baechler SA, Redon CE, Zhang H, et al. SLFN11 blocks stressed replication forks independently of ATR. Mol Cell. 2018;69:371–.e6. https://doi.org/10.1016/j.molcel.2018.01.012 ."), [3](https://www.nature.com/articles/s41416-026-03571-2#ref-CR3 "Nogales V, Reinhold WC, Varma S, Martinez-Cardus A, Moutinho C, Moran S, et al. Epigenetic inactivation of the putative DNA/RNA helicase SLFN11 in human cancer confers resistance to platinum drugs. Oncotarget. 2015;7:3084–97. https://doi.org/10.18632/oncotarget.6413 .")], leading to the opening of the chromatin around the replication initiation sites, which activates the transcription of immediate early genes that can induce cell cycle arrest. Thereby blocking any further replications from occurring [[4](https://www.nature.com/articles/s41416-026-03571-2#ref-CR4 "Murai J, Zhang H, Pongor L, Tang S-W, Jo U, Moribe F, et al. Chromatin remodeling and immediate early gene activation by SLFN11 in response to replication stress. Cell Rep. 2020;30:4137–.e6. https://doi.org/10.1016/j.celrep.2020.02.117 .")]. This is done independently of, and in parallel with, the ATR-CHEK 1 S-phase checkpoint in the DDR pathway [[2](https://www.nature.com/articles/s41416-026-03571-2#ref-CR2 "Murai J, Tang S-W, Leo E, Baechler SA, Redon CE, Zhang H, et al. SLFN11 blocks stressed replication forks independently of ATR. Mol Cell. 2018;69:371–.e6. https://doi.org/10.1016/j.molcel.2018.01.012 .")]. Given the frequent defects in the DDR pathway observed in cancers [[5](https://www.nature.com/articles/s41416-026-03571-2#ref-CR5 "Knijnenburg TA, Wang L, Zimmermann MT, Chambwe N, Gao GF, Cherniack AD, et al. Genomic and molecular landscape of DNA damage repair deficiency across the cancer genome atlas. Cell Rep. 2018;23:239–254.e6. https://doi.org/10.1016/j.celrep.2018.03.076 .")], SLFN11 may serve as a critical fail-safe mechanism for inducing cell cycle arrest in response to DNA damage. SLFN11 expressions are tightly regulated at the epigenetic and transcriptional levels. In cancer cells, SLFN11 is frequently silenced through promoter methylation, resulting in resistance to DDAs and PARP inhibitors [[2](https://www.nature.com/articles/s41416-026-03571-2#ref-CR2 "Murai J, Tang S-W, Leo E, Baechler SA, Redon CE, Zhang H, et al. SLFN11 blocks stressed replication forks independently of ATR. Mol Cell. 2018;69:371–.e6. https://doi.org/10.1016/j.molcel.2018.01.012 ."), [3](https://www.nature.com/articles/s41416-026-03571-2#ref-CR3 "Nogales V, Reinhold WC, Varma S, Martinez-Cardus A, Moutinho C, Moran S, et al. Epigenetic inactivation of the putative DNA/RNA helicase SLFN11 in human cancer confers resistance to platinum drugs. Oncotarget. 2015;7:3084–97. https://doi.org/10.18632/oncotarget.6413 ."), [6](https://www.nature.com/articles/s41416-026-03571-2#ref-CR6 "Murai J, Thomas A, Miettinen M, Pommier Y. Schlafen 11 \(SLFN11\), a restriction factor for replicative stress induced by DNA-targeting anti-cancer therapies. Pharm Ther. 2019;201:94–102. https://doi.org/10.1016/j.pharmthera.2019.05.009 ."), [7](https://www.nature.com/articles/s41416-026-03571-2#ref-CR7 "Tlemsani C, Pongor L, Elloumi F, Girard L, Huffman KE, Roper N, et al. SCLC-CellMiner: a resource for small cell lung cancer cell line genomics and pharmacology based on genomic signatures. Cell Rep. 2020;33:108296. https://doi.org/10.1016/j.celrep.2020.108296 .")]. In a study of 66 human small cell lung cancer (SCLC) cell lines, higher promoter methylation correlated with reduced SLFN11 expression and treatment resistance [[7](https://www.nature.com/articles/s41416-026-03571-2#ref-CR7 "Tlemsani C, Pongor L, Elloumi F, Girard L, Huffman KE, Roper N, et al. SCLC-CellMiner: a resource for small cell lung cancer cell line genomics and pharmacology based on genomic signatures. Cell Rep. 2020;33:108296. https://doi.org/10.1016/j.celrep.2020.108296 .")]. Three main mechanisms suppress SLFN11 gene expression: promoter methylation, histone methylation by the Polycomb Repressive Complex (PRC) and histone deacetylation [[2](https://www.nature.com/articles/s41416-026-03571-2#ref-CR2 "Murai J, Tang S-W, Leo E, Baechler SA, Redon CE, Zhang H, et al. SLFN11 blocks stressed replication forks independently of ATR. Mol Cell. 2018;69:371–.e6. https://doi.org/10.1016/j.molcel.2018.01.012 ."), [3](https://www.nature.com/articles/s41416-026-03571-2#ref-CR3 "Nogales V, Reinhold WC, Varma S, Martinez-Cardus A, Moutinho C, Moran S, et al. Epigenetic inactivation of the putative DNA/RNA helicase SLFN11 in human cancer confers resistance to platinum drugs. Oncotarget. 2015;7:3084–97. https://doi.org/10.18632/oncotarget.6413 ."), [8](https://www.nature.com/articles/s41416-026-03571-2#ref-CR8 "Stewart CA, Tong P, Cardnell RJ, Sen T, Li L, Gay CM, et al. Dynamic variations in epithelial-to-mesenchymal transition \(EMT\), ATM, and SLFN11 govern response to PARP inhibitors and cisplatin in small cell lung cancer. Oncotarget. 2017;8:28575–87. https://doi.org/10.18632/oncotarget.15338 ."), [9](https://www.nature.com/articles/s41416-026-03571-2#ref-CR9 "Tang S-W, Thomas A, Murai J, Trepel JB, Bates SE, Rajapakse VN, et al. Overcoming resistance to DNA-targeted agents by epigenetic activation of Schlafen 11 \(SLFN11\) expression with class I histone deacetylase inhibitors. Clin Cancer Res. 2018;24:1944–53. https://doi.org/10.1158/1078-0432.CCR-17-0443 .")]. SLFN11 is also regulated by interferon-gamma (IFN-γ), linking it to the innate immune response. IFN-γ, crucial for immune defence, induces SLFN11, which can predict sensitivity to treatments like Olaparib and Temozolomide in SCLC [[10](https://www.nature.com/articles/s41416-026-03571-2#ref-CR10 "Mavrommatis E, Fish EN, Platanias LC. The schlafen family of proteins and their regulation by interferons. J Interferon Cytokine Res. 2013;33:206–10. https://doi.org/10.1089/jir.2012.0133 ."),[11](https://www.nature.com/articles/s41416-026-03571-2#ref-CR11 "Stark GR, Kerr IM, Williams BR, Silverman RH, Schreiber RD. How cells respond to interferons. Annu Rev Biochem. 1998;67:227–64. https://doi.org/10.1146/annurev.biochem.67.1.227 ."),[12](https://www.nature.com/articles/s41416-026-03571-2#ref-CR12 "Farago AF, Yeap BY, Stanzione M, Hung YP, Heist RS, Marcoux JP, et al. Combination olaparib and temozolomide in relapsed small-cell lung cancer. Cancer Discov. 2019;9:1372–87. https://doi.org/10.1158/2159-8290.CD-19-0582 ."),[13](https://www.nature.com/articles/s41416-026-03571-2#ref-CR13 "Pacheco JM, Byers LA. Temozolomide plus PARP inhibition in small-cell lung cancer: could patient-derived xenografts accelerate discovery of biomarker candidates?. Cancer Discov. 2019;9:1340–2. https://doi.org/10.1158/2159-8290.CD-19-0850 .")]. Additionally, SLFN11 induction during viral infections, such as Zika virus or HIV, correlates with viral inhibition, suggesting a shared pathway between innate immune activation and DDA response [[14](https://www.nature.com/articles/s41416-026-03571-2#ref-CR14 "Li M, Kao E, Gao X, Sandig H, Limmer K, Pavon-Eternod M, et al. Codon-usage-based inhibition of HIV protein synthesis by human Schlafen 11. Nature. 2012;491:125–8. https://doi.org/10.1038/nature11433 .")]. While most studies on SLFN11 have focused on adult cancers, our investigation explores its role as a predictive biomarker in paediatric cancers, which often exhibit distinct genetic and molecular characteristics. Conflicting results were reported in the literature regarding SLFN11 and response to DNA Damage agents. For instance, in Ewing sarcoma, SLFN11 is upregulated by the EWS-FLI1 fusion and correlates with better response to PARP inhibitors and improved survival [[15](https://www.nature.com/articles/s41416-026-03571-2#ref-CR15 "Tang S-W, Bilke S, Cao L, Murai J, Sousa FG, Yamade M, et al. SLFN11 is a transcriptional target of EWS-FLI1 and a determinant of drug response in Ewing’s sarcoma. Clin Cancer Res. 2015;21:4184 https://doi.org/10.1158/1078-0432.CCR-14-2112 .")]. In medulloblastoma, especially WNT and SHH subtypes, high SLFN11 enhances cisplatin sensitivity and can be upregulated with HDAC inhibitors [[16](https://www.nature.com/articles/s41416-026-03571-2#ref-CR16 "Nakata S, Murai J, Okada M, Takahashi H, Findlay TH, Malebranche K, et al. Epigenetic upregulation of Schlafen11 renders WNT- and SHH-activated medulloblastomas sensitive to cisplatin. Neuro-Oncol. 2022;25:899–912. https://doi.org/10.1093/neuonc/noac243 .")]. A pan-cancer analysis showed SLFN11 expression in 69% of paediatric solid tumours, notably in Ewing sarcoma (90%) and desmoplastic small round-cell tumours (100%). While SLFN11 predicts DDA response in preclinical models, clinical outcomes suggest additional factors may influence its predictive value.[[17](https://www.nature.com/articles/s41416-026-03571-2#ref-CR17 "Gartrell J, Mellado-Largarde M, Clay MR, Bahrami A, Sahr NA, Sykes A, et al. SLFN11 is widely expre
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